Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sumatriptan”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,765 records · Page 98Linked to original sources

Management of treatment resistant obsessive-compulsive disorder. Algorithms for pharmacotherapy.

Treatment resistant OCD subjects, defined as those patients who undergo an adequate trial of SRI (clomipramine or SSRI) and do not respond or show unsatisfactory results, account for 40-50% of all patients. Once the appropriateness of the trial has been assessed, several options exist for the clinicians. If clomipramine or citalopram have been used, an appropriate strategy consists in giving the same drug intravenously. Double-blind studies exist on the efficacy of clomipramine IV, while data are missing for citalopram. Another option that should be considered first, although data are scarce, is the addition of a cognitive behavioral therapy, when available, in the forms of exposure and response prevention. When such options are not suitable or available, augmentation of the ongoing SRI with another compound represents the preferable strategy. Double-blind, placebo-controlled studies have shown the efficacy of adding pindolol (7.5 mg/d), risperidone (2 mg/d) and olanzapine (5-10 mg/d). Other agents have been proposed, but data emerging from double-blind studies were negative or contradictory. Another option available is switching from CMI to SSRI, or vice versa, or from SSRI to SSRI. Data regarding such treatment strategy, however, are highly preliminary, based on a couple of open label reports and on studies performed in treatment resistant depression. An unresolved question is whether augmentation should be preferred to switching. No data exist in OCD; a practical approach would suggest augmentation first, considering that response should be obtained faster than by switching compound. When all the available and effective strategies prove uneffective, clinicians should consider switching the patient to other compounds in monotherapy, such as venlafaxine, sumatriptan, inositol, although research is strongly needed before conclusions on the efficacy of such compounds can be drawn.

Algorithms↗

[Serotonin syndrome. Several cases of this often overlooked diagnosis].

During the recent decade an increasing number of inquiries concerning cases of overdoses exhibiting typical signs of the serotonin syndrome have been recorded at the Swedish Poisons Information Centre. Four of these cases are presented together with a review of the literature. All patients had overdosed moclobemide and in one case this was the only drug taken. The other patients had ingested moclobemide together with citalopram (2 cases) and clomipramine (1 case). Moreover, other serotoninergic pharmaceuticals as sertraline and sumatriptan were simultaneously ingested in one case and buspirone in another. Three of the cases had hyperthermia, > 40 degrees C and the same number showed pronounced muscle rigidity, coma and mydriasis. Other severe signs and symptoms upon admission included positive Babinski and trismus in two cases each and seizures in one. All patients received mechanical ventilation. Two were treated with dantrolene sodium and one of them was given cyproheptadine as well. One patient received cyproheptadine treatment alone and another prolonged muscle relaxation. Three patients had a typical short clinical course, whereas one patient developed rhabdomyolysis, DIC and arrhythmias. All patients fully recovered.

Adult↗

Gateways to Clinical Trials.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the world's first drug discovery and development portal, and provides information on study design, treatments, conclusions and references. This issue focuses on the following selection of drugs: Abiciximab, acetylcholine chloride, acetylcysteine, alefacept, alemtuzumab, alicaforsen, alteplase, aminopterin, amoxicillin sodium, amphotericin B, anastrozole, argatroban monohydrate, arsenic trioxide, aspirin, atazanavir, atorvastatin, augmerosen, azathioprine; Benzylpenicillin, BMS-284756, botulinum toxin type A, botulinum toxin type B, BQ-123, budesonide, BXT-51072; Calcium folinate, carbamazepine, carboplatin, carmustine, ceftriaxone sodium, cefuroxime axetil, chorionic gonadotropin (human), cimetidine, ciprofloxacin hydrochloride, cisplatin, citalopram hydrobromide, cladribine, clarithromycin, clavulanic acid, clofarabine, clopidogrel hydrogensulfate, clotrimazole, CNI-1493, colesevelam hydrochloride, cyclophosphamide, cytarabine; Dalteparin sodium, daptomycin, darbepoetin alfa, debrisoquine sulfate, dexrazoxane, diaziquone, didanosine, docetaxel, donezepil, doxorubicin hydrochloride liposome injection, DX-9065a; Eberconazole, ecogramostim, eletriptan, enoxaparin sodium, epoetin, epoprostenol sodium, erlizumab, ertapenem sodium, ezetimibe; Fampridine, fenofibrate, filgrastim, fluconazole, fludarabine phosphate, fluorouracil, 5-fluorouracil/epinephrine, fondaparinux sodium, formoterol fumarate; Gabapentin, gemcitabine, gemfibrozil, glatiramer; Heparin sodium, homoharringtonine; Ibuprofen, iloprost, imatinib mesilate, imiquimod, interferon alpha-2b, interferon alpha-2c, interferon-beta; KW-6002; Lamotrigine, lanoteplase, metoprolol tartrate, mitoxantrone hydrochloride; Naproxen sodium, naratriptan, Natalizumab, nelfinavir mesilate, nevirapine, nifedipine, NSC-683864; Oral heparin; Paclitaxel, peginterferon alfa-2b, phenytoin, pimecrolimus, piperacillin, pleconaril, pramipexole hydrochloride, prednisone, pregabalin, progesterone; Rasburicase, ravuconazole, reteplase, ribavirin, rituximab, rizatriptan, rosiglitazone maleate, rotigotine; Semaxanib, sildenafil citrate, simvastatin, stavudine, sumatriptan; Tacrolimus, tamoxifen citrate, tanomastat, tazobactam, telithromycin, tenecteplase, tolafentrine, tolterodine tartrate, triamcinolone acetonide, trimetazidine, troxacitabine; Valproic acid, vancomycin hydrochloride, vincristine, voriconazole, Warfarin sodium; Ximelagatran, Zidovudine, zolmitriptan.

Clinical Trials as Topic↗

Gateways to Clinical Trials. June 2002.

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies knowledge area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: Abacavir sulfate, abarelix, abciximab, alicaforsen sodium, almotriptan, alteplase, amlodipine, amoxicillin trihydrate, amprenavir, argatroban monohydrate, aspirin, atorvastatin calcium, azathioprine; Baclofen, benidipine hydrochloride, benserazide, BMS-214662, bosentan, botulinum toxin type B; Candesartan cilexetil, carbamazepine, carbidopa, carboplatin, ceftriaxone sodium, celecoxib, cetirizine hydrochloride, clarithromycin, clavulanate potassium, clopidogrel hydrogensulfate, clozapine, CPI-1189, cyclophosphamide, cytarabine; Darbepoetin alfa, denileukin diftitox, dexamethasone, dipyridamole, droperidol, DW-166HC; Ebastine, efalizumab, efavirenz, eletriptan, enalapril maleate, enfuvirtide, enoxaparin sodium, enrasentan, entacapone, epoetin, eprosartan mesilate, etanercept, etoricoxib; Fenofibratefexofenadine hydrochloride, filgrastim, fludarabine phosphate, fluoxetine hydrochloride fluvoxamine maleate, frovatriptan, furosemide; Gabapentin, galantamine hydrobromide, gatifloxacin, gefitinib, ghrelin (human), glatiramer acetate; Haloperidol; Ibuprofen, ibuprofen, guaiacol ester, idarubicin hydrochloride, imipramine hydrochloride, imiquimod, interferon beta, interferon beta-1a, interferon beta-1b, interferon omega, irbesartan, itraconazole; Ketorolac, ketorolac tromethamine; Lamifiban, lamotrigine, lanoteplase, lansoprazole, leflunomide, leuprorelin acetate, levetiracetam, levocetirizine, levodopa, lisinopril, loratadine; Manidipine, methylprednisolone, metronidazole, mirtazapine, mizolastine, modafinil, morphine sulfate; Naproxen sodium, naratriptan hydrochloride, nifedipine, NSC-683864; Ofloxacin, olanzapine, omalizumab, omapatrilat, ondansetron hydrochloride, oxcarbazepine; Paclitaxel, parecoxib sodium, paroxetine hydrochloride, phenytoin sodium, pimecrolimus, pramipexole hydrochloride, pravastatin, prednisone, pregabalin; Quetiapine fumarate; Ranitidine hydrochloride, rasburicase, ritonavir, rivastigmine tartrate, rizatriptan benzoate, rofecoxib; Saquinavir mesilate, sertraline, sildenafil citrate, simvastatin, sumatriptan succinate; Tacrolimus, tiagabine hydrochloride, ticlopidine hydrochloride, tirofiban hydrochloride, tolvaptan, topiramate, tretinoin; Valproic acid, valsartan, venlafaxine hydrochloride, verapamil; Warfarin sodium; Ximelagatran; Zanamivir, ziconotide, zolmitriptan, zonisamide.

Drug Therapy↗

Selegiline: a second look. Six years later: too risky in Parkinson's disease.

(1) The reference treatment for Parkinson's disease is levodopa plus a peripheral dopadecarboxylase inhibitor (benserazide or carbidopa). (2) In 1996, selegiline, a type B MAOI marketed in France since 1988, saw its indications extended to cover single-agent therapy of early-stage Parkinson's disease, and in combination with levodopa, before onset of complications of levodopa therapy. The initial clinical file failed to show that selegiline had any benefit in these indications. (3) Now, in 2002, new data from trials involving hundreds of untreated patients show that selegiline postpones the need for levodopa therapy for a few months but fails to substantially alter the progression of Parkinson's disease. (4) A clinical trial and a retrospective epidemiological study of patients with advanced Parkinson's disease showed excess mortality on selegiline. (5) The side effects of selegiline are similar to those of other antiparkinsonian drugs and amphetamine. Notable side effects include cardiovascular problems (postural hypotension, atrial fibrillation and arterial hypertension). (6) Selegiline can cause a serotoninergic syndrome and arterial hypertension, so must not be combined with pethidine, tramadol, bupropion, sumatriptan, zolmitriptan or naratriptan. Concurrent treatment with serotonin reuptake inhibitor antidepressants should also be avoided. (7) Given the only moderate effects of selegiline in Parkinson's disease, and the possibility of a slight increase in mortality, there is no justification for prescribing this medication in patients with Parkinson's disease. (8) Whatever the stage of Parkinson's disease, there is no justification for starting patients on selegiline. Patients who are already taking selegiline should only continue to take it if they feel a clear benefit and are free from risk factors for early mortality, especially cardiovascular disease.

Antiparkinson Agents↗

Eletriptan Pfizer.

Pfizer has developed and launched eletriptan, a 5-HT1B/1D agonist, for the potential treatment of migraine with and without aura. Eletriptan has 6-fold greater affinity for the 5-HT1D receptor than sumatriptan, and a 3-fold greater affinity for the 5-HT1B receptor [249570]. Eletriptan pharmacology has also been evaluated in vitro in comparison with zolmitriptan (AstraZeneca plc) and naratriptan (GlaxoSmithKline plc) [290116].

Animals↗

[Serotonin syndrome--several cases of this often overlooked diagnosis].

During the recent decade an increasing number of inquiries concerning cases of overdoses exhibiting typical signs of the serotonin syndrome have been recorded at the Swedish Poisons Information Centre. Four of these cases are presented together with a review of the literature. All patients had overdosed moclobemide and in one case this was the only drug taken. The other patients had ingested moclobemide together with citalopram (2 cases) and clomipramine (1 case). Moreover, other serotoninergic pharmaceuticals as sertraline and sumatriptan were simultaneously ingested in one case and buspirone in another. Three of the cases had hyperthermia, > 40 degrees C and the same number showed pronounced muscle rigidity, coma and mydriasis. Other severe signs and symptoms upon admission included positive Babinski and trismus in two cases each and seizures in one. All patients received mechanical ventilation. Two were treated with dantrolene sodium and one of them was given cyproheptadine as well. One patient received cyproheptadine treatment alone and another prolonged muscle relaxation. Three patients had a typical short clinical course, whereas one patient developed rhabdomyolysis, DIC and arrhythmias. All patients fully recovered.

Adult↗

Update on the role of drug therapy in non-ulcer dyspepsia.

Non-ulcer dyspepsia is common and is often confused with other diagnoses. It remains a condition identified by exclusion, and continues to be a challenge to manage. Currently, only a limited number of pharmacological options are available. Antacids are no more effective than placebo in treating nonulcer dyspepsia. H2-receptor antagonists appear to be superior to placebo in efficacy, but many of the studies suggesting this finding have had a suboptimal study design. Proton pump inhibitors have been shown to be superior to placebo, although questions remain as to whether the only subgroup that responds is comprised of patients with unrecognized gastroesophageal reflux disease. Studies have found that prokinetic agents are superior to placebo, but currently only a very limited number of agents within this class can be prescribed in the United States. Sparse data support the role of metoclopramide and its side effects limit its use even further. The eradication of Helicobacter pylori has a small but positive therapeutic benefit in non-ulcer dyspepsia, and can be considered in those confirmed to be infected. Sucralfate is unlikely to be effective, and misoprostol is ineffective. Bismuth alone is probably not efficacious. Tricyclic antidepressants may have a therapeutic role, but this is not firmly established and this class of medication should be reserved for resistant cases. Emerging therapies include drugs that relax the gastric fundus, such as buspirone or sumatriptan, and the new prokinetic tegaserod. Psychological therapies may play a role but studies of these therapies are limited. Therapy for non-ulcer dyspepsia remains challenging and is usually empiric; it will remain so until the mechanisms that induce symptoms of dyspepsia are better understood.

Anti-Ulcer Agents↗

[A review of the pharmacologic treatment of migraine in children].

OBJECTIVE: To describe the efficacy and tolerability of the different medications used to treat migraine in children and adolescents. DEVELOPMENT: A literature review of the drug studies involving children and adolescents for the treatment of migraine was conducted. The treatment of migraine is divided into abortive and prophylactic. The different classes of drugs are described in respect to its efficacy and side effects. Few placebo-controlled, double-blind studies are available in children as compared to adults for the treatment of migraine headaches. Only ibuprofen and nasal sumatriptan have been studied and shown to be effective in more than one double blind placebo-controlled study for the abortive treatment of migraine in children. Unlike the adult studies, the oral triptans tested in children have not been effective when compared to placebo. Only flunarizine has shown efficacy in more than one placebo controlled trial for the prophylactic treatment. CONCLUSION: Most of the medications used to treat migraine in children and adolescents are well tolerated. The treatment response of migraine in children and adolescents may differ from that of adults. There seems to be a high placebo response rate in the pediatric population. Therefore, further prospective placebo-controlled studies are needed.

Adolescent↗

[The pathogenetic bases of hemicrania].

Studies of regional cerebral blood flow in migraine with aura have shown that the aura phase is associated with hypoperfusion in the cortical area which relates topographically to the clinical symptoms. Thus, the previously hypoperfused area becomes hyperperfused. However, there is no strict association between hyperperfusion and headache. The mode of hypoperfusion propagation recalls the circulatory manifestations of experimental cortical spreading depression. In addition, there are no focal cerebral blood flow abnormalities in migraine without aura. During the headache phase of migraine, dilation of both the large extra- and intracranial arteries takes place. A bulk of biochemical evidence has suggested that the pain in migraine is caused by blood vessels which are dilated and sensitized by circulating pain-producing substances e.g. bradykinin, serotonin and histamine (sterile inflammation). Recently, perivascular trigeminal fibres (trigeminovascular system) which, when stimulated, release sensory peptides (substance P and the calcitonin gene-related peptide) capable of provoking marked vasodilation and plasma extravasation (neurogenic inflammation) have been identified. Thus, the activation of the trigeminovascular system is probably involved in the vasodilatative and nociceptive phenomena of the migraine attack. The finding of a reduced endorphinergic brain tonus in migraine patients supports the hypothesis of a central nociceptive derangement in migraine. Nonetheless, the exact relationship between vasodilation and headache remains to be defined. However, the potent antimigraine effectiveness of sumatriptan--an agonist of the serotonin receptors which selectively constricts dilated arteries during the migraine attack--once again stresses the fact that serotonin is probably the crucial factor in the link between vasodilation and headache.

Cerebrovascular Circulation↗

Cloning and pharmacological characterization of a novel human 5-hydroxytryptamine1D receptor subtype.

The canine RDC4 gene was used to isolate two distinct human serotonin receptor genes. The receptor encoded by clone RH-6 was the species homolog of RDC4 and was identical to a human serotonin 5-hydroxytryptamine1D (5-HT1D) receptor that was recently reported [Mol. Pharmacol. 40:143-148 (1991)]. The receptor encoded by RH-2 was a novel 5-HT receptor that was 61% identical to RH-6 and showed the greatest homology with the rat 5-HT1B receptor sequence (94%). The RH-2 gene contained an intronless, 1170-base pair, open reading frame that encoded a 390-amino acid protein that contained all of the hallmarks of a guanine nucleotide-binding protein-linked receptor. Heterologous expression of the RH-2 gene in Chinese hamster ovary cells led to the appearance of high affinity binding sites for 5-HT (Kd = 2.6 nM, Bmax = 2.9 pmol/mg of membrane protein), and the receptor expressed in Chinese hamster ovary cells was coupled to inhibition of adenylyl cyclase. Competition binding experiments using compounds that are selective for various 5-HT receptor subtypes showed the highest correlation with a 5-HT1D-like receptor (r = 0.89) and a low correlation with 5-HT1B-like receptors. Examples of the 5-HT1D-like pharmacology displayed by RH-2 include high affinity for the 5-HT1D-selective compound sumatriptan (Ki = 9.4 nM) and for the alpha 2-adrenergic receptor antagonist rauwolscine (Ki = 47 nM). Therefore, despite the close genetic relationship between RH-2 and the rat 5-HT1B receptor, our results indicate that the receptor encoded by RH-2 2 is best classified as a human 5-HT1D receptor subtype and defines a second member of the human 5-HT1D receptor family.

Amino Acid Sequence↗

Serotonin-induced relaxation in canine coronary artery smooth muscle.

Serotonin (5-HT) is a potent contractile agonist in canine coronary artery devoid of endothelium; however, in higher concentrations 5-HT produces concentration-dependent relaxation by activating an as yet uncharacterized receptor. This study explored the possibility that 5-HT-induced relaxation was mediated by interaction with a member of the 5-HT1, 5-HT2, 5-HT3, or 5-HT4 receptor family. 5-HT, 5-carboxamidotryptamine and 5-methoxytryptamine produced concentration-dependent relaxation in vitro in tissues precontracted with prostaglandin F2 alpha (10 microM). The agonist rank order potency for relaxation was 5-carboxamidotryptamine > 5-HT > 5-MeOT. 8-hydroxydipropylaminotetralin (8-OH-DPAT), dipropyl-5-CT, 5-methyltryptamine, sumatriptan, alpha-methyl-5-HT and 2-methyl-5-HT did not produce significant relaxation. The 5-HT1/beta adrenergic receptor antagonist propranolol (1 microM) did not antagonize 5-HT-induced relaxation. 5-HT-induced relaxation was not blocked by tetrodotoxin (0.3 microM), suggesting that neuronal depolarization to release mediators from nerves was not responsible for the relaxation. Neither ketanserin (1 microM) nor ritanserin (1 microM) antagonized 5-HT-induced relaxation, suggesting that 5-HT2 and 5-HT1C receptors do not mediate relaxation. ICS 205-930 (10 microM), a 5-HT3/5-HT4 receptor antagonist, shifted the 5-HT concentration-response curve modestly to the right (pKB = 5.1 +/- 0.1). Cisapride, a 5-HT4 receptor agonist, was not effective either as an agonist (up to 10 microM), or as an antagonist (1 microM) of 5-HT-induced relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Evidence for a 5-HT1-like receptor mediating the amplifying action of 5-HT in the rabbit ear artery.

1. The nature of the 5-hydroxytryptamine (5-HT) receptors which amplify the vasoconstrictor effect of methoxamine was examined in the rabbit isolated perfused ear artery with intact endothelium. Indices of amplification were leftward shifts of methoxamine dose-response (DR) curves produced by 5-HT (0.3 microM) (Method I), and the appearance of vasoconstrictor responses to 5-HT receptor agonists when methoxamine was present in a near-threshold concentration (Method II). 2. The amplifying effect of 5-HT (Method I) was unaffected by prazosin (0.08 microM), was partly depressed by 5-HT2-receptor antagonists in high concentrations (ketanserin 0.5 microM, LY53857, 1.0 microM), and was abolished by a non-selective antagonist of 5-HT1 and 5-HT2 receptors (methiothepin, 0.01 microM). 3. Amplifying potencies of agonists assessed by both Methods I and II were in the order 5-carbox-amidotryptamine (5-CT) greater than 5-HT greater than alpha-methyl 5-HT. The potency of sumatriptan (assessed by Method II only) was intermediate between those of 5-HT and alpha-methyl 5-HT. 4. Ketanserin and LY53857 inhibited the amplifying action of 5-CT to about the same extent as that of 5-HT. 5. The amplifying potencies of the agonists are in marked contrast to the reported contractile potencies in the rabbit aorta where the receptor is 5-HT2, but are almost identical with reported contractile potencies in the dog saphenous vein where the receptor is 5-HT1-like. 6. It is concluded that a 5-HT,-like receptor mediates the amplifying interaction between 5-HT and methoxamine in the rabbit ear artery which can be weakly blocked by ketanserin and LY53857.7. Since 5-CT was equipotent when applied separately to the intimal and adventitial surfaces of the artery, it is suggested that the 5-HT,-like receptors are distributed uniformly across the artery wall.

Acetylcholine↗

Chronic headaches in family practice.

BACKGROUND: More than 11 million people in the United States have moderate or severe migraine resulting in much suffering and millions of lost work days annually. Staying abreast of current advances in headache management is important for family physicians, who care for most headache patients. METHODS: MEDLINE files were searched from 1982 to the present using the key words "headache," "migraine," "serotonin," and "cerebral circulation." Also searched were the journals Headache and Cephalalgia and the published proceedings of meetings of the American Association for the Study of Headache, the International Headache Society, and the Migraine Trust. RESULTS AND CONCLUSIONS: A new headache classification based on clinical symptoms has been published by the International Headache Society, which clarifies headache diagnoses. Though headaches with serious underlying disease occur only rarely in family practice, physicians must be familiar with the clinical signs indicating the presence of such problems, and any change in or unusual presentation of headache warrants investigation. Headache research has expanded in the past decade, much of which has been directed at raising the standards of treatment. Pharmacologic treatment falls into two categories: acute or abortive treatment and preventive treatment. Analgesic overmedication by headache patients is commonplace and leads to withdrawal symptoms and the development of chronic daily headaches, for which effective treatments are now available at both ambulatory and inpatient levels. At the more basic research level, serotonin receptor studies have provided an impetus for revealing underlying headache mechanisms. A new serotonin agonist, sumatriptan, has proved effective in treating acute migraine and will no doubt be followed by further serotonergic drugs. Patient education, relaxation therapy, and other nonpharmacological approaches, as well as good overall standards of care, are essential ingredients in headache management. Family physicians are well-equipped to offer these approaches to their patients with headache.

Child↗

[Cluster headache].

Cluster headache is characterized by recurrent unilateral attacks of headache of great intensity and brief duration (15-180 minutes), accompanied by local signs and symptoms of autonomic dysfunction including conjunctival injection, lacrimation, nasal congestion, rhinnorrhea, forehead and facial sweating, miosis, ptosis or eyelid edema. Attacks occur in so-called cluster periods lasting for weeks or months. About 10% of patients have chronic symptoms with no period of remission. There are only two abortive treatments with proven efficacy: subcutaneous sumatriptan and nasal oxygen inhalation. Prophylactic treatment is often needed to reduce the daily frequency of attacks: verapamil in episodic cluster headache and lithium in chronic cluster headache.

Cluster Headache↗

[Trigemino-autonomic cephalalgias. Report of two cases].

Trigemino-autonomic cephalalgias (TAC) constitute a rare group of primary headache conditions associated with unilateral fluctuating head pain and autonomic symptoms. These syndromes, including cluster headache, hemicrania continua, paroxysmal hemicrania and SUNCT, are much less prevalent than migraine and tension-type headache. The pathogenesis of TAC is unknown. Similar neuropeptide changes seen in all TAC syndromes suggest a shared underlying pathophysiology in these headaches. Some of them respond to the treatment with indomethacin and sumatriptan. Two patients suffering from one of the trigemino-autonomic cephalalgias are presented in the paper.

Adult↗

New thoughts on sinus headache.

Sinus headache is not a recognized entity by allergy, otolaryngology, or neurological organizations. Headache is a minor feature in the diagnosis of acute rhinosinusitis and is not validated as a symptom in chronic sinusitis. Sinus headaches are self-diagnosed due to weather triggers, bilateral and frontomaxillary location, and the presence of vasomotor signs and symptoms, all of which can accompany the migraine. Over 90% of self-diagnosed and doctor-diagnosed sinus headaches meet the International Headache Society criteria for migraines, and those migraines misdiagnosed as sinus headaches respond to sumatriptan better than placebo because migraines respond to triptans. Sinus headaches are usually severely disabling migraines, misdiagnosed and mistreated, with 61% of patients receiving antibiotic prescriptions for noninfectious causes, thus failing the patients and, in addition, contributing to a serious public health problem.

Headache↗