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PubMed2006

Nitric oxide regulation of calcitonin gene-related peptide gene expression in rat trigeminal ganglia neurons.

Calcitonin gene-related peptide (CGRP) and nitric oxide are involved in the underlying pathophysiology of migraine and other diseases involving neurogenic inflammation. We have tested the hypothesis that nitric oxide might trigger signaling mechanisms within the trigeminal ganglia neurons that would coordinately stimulate CGRP synthesis and release. Treatment of primary trigeminal ganglia cultures with nitric oxide donors caused a greater than four-fold increase in CGRP release compared with unstimulated cultures. Similarly, CGRP promoter activity was also stimulated by nitric oxide donors and overexpression of inducible nitric oxide synthase (iNOS). Cotreatment with the antimigraine drug sumatriptan greatly repressed nitric oxide stimulation of CGRP promoter activity and secretion. Somewhat surprisingly, the mechanisms of nitric oxide stimulation of CGRP secretion did not require cGMP or PI3-kinase signaling pathways, but rather, nitric oxide action required extracellular calcium and likely involves T-type calcium channels. Furthermore, nitric oxide was shown to increase expression of the active forms of the mitogen-activated protein kinases Jun amino-terminal kinase and p38 but not extracellular signal-related kinase in trigeminal neurons. In summary, our results provide new insight into the cellular mechanisms by which nitric oxide induces CGRP synthesis and secretion from trigeminal neurons.

Animals↗
PubMed2005

Multiple attack study on the available triptans in Italy versus placebo.

The aim of the study is to evaluate the efficacy and tolerability of the five triptans that are commercially available in Italy (zolmitriptan 2.5 mg, rizatriptan 10 mg, sumatriptan 100 mg, almotriptan 12.5 mg and eletriptan 40 mg). The study was conducted in single-blind versus placebo and its duration was 18 months. At the Headache Centre of the 'Agostino Gemelli' Hospital in Rome we selected 42 patients, suffering from headache with and without aura (International Headache Society Committee on Headache Classification, 1988 Cephalalgia 8:1-96), whose headache frequency ranged between 1- and 4-monthly crises. For a total of 25 crises, for every five consecutive crises, a different triptan was taken. The end-points of the study were as follows: response at 2 h, 'pain free' at 2 h and 'sustained pain free' (at 24 h). The intra-patient consistency and the tolerability were also evaluated. Thirty patients completed the study and the statistical analysis was only applied to these patients. No substantial difference in terms of the efficacy of the triptans was noted; all triptans were well tolerated. These results suggest the possibility of testing different triptans in the same patient in order to identify the ideal drug for every patient.

Adult↗
PubMed2006

EFNS guidelines on the treatment of cluster headache and other trigeminal-autonomic cephalalgias.

Cluster headache and the other trigeminal-autonomic cephalalgias [paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) syndrome] are rare but very disabling conditions with a major impact on the patient's quality of life. The objective of this study was to give evidence-based recommendations for the treatment of these headache disorders based on a literature search and consensus amongst a panel of experts. All available medical reference systems were screened for any kind of studies on cluster headache, paroxysmal hemicrania and SUNCT syndrome. The findings in these studies were evaluated according to the recommendations of the European Federation of Neurological Societies resulting in level A, B or C recommendations and good practice points. For the acute treatment of cluster headache attacks, oxygen (100%) with a flow of at least 7 l/min over 15 min and 6 mg subcutaneous sumatriptan are drugs of first choice. Prophylaxis of cluster headache should be performed with verapamil at a daily dose of at least 240 mg (maximum dose depends on efficacy or tolerability). Although no class I or II trials are available, steroids are clearly effective in cluster headache. Therefore, the use of at least 100 mg methylprednisone (or equivalent corticosteroid) given orally or at up to 500 mg i.v. per day over 5 days (then tapering down) is recommended. Methysergide, lithium and topiramate are recommended as alternative treatments. Surgical procedures, although in part promising, require further scientific evaluation. For paroxysmal hemicranias, indomethacin at a daily dose of up to 225 mg is the drug of choice. For treatment of SUNCT syndrome, large series suggest that lamotrigine is the most effective preventive agent, with topiramate and gabapentin also being useful. Intravenous lidocaine may also be helpful as an acute therapy when patients are extremely distressed and disabled by frequent attacks.

Advisory Committees↗
PubMed2004

Double-blind clinical trials of oral triptans vs other classes of acute migraine medication - a review.

Although the migraine clinical trials literature is enormous, we identified only nine published double-blind studies which compare an oral triptan with a non-triptan acute treatment. Of the nine comparative trials that met inclusion criteria for this review, six compared sumatriptan with other drugs, zolmitriptan was studied in two trials and eletriptan in one trial. In seven of the nine studies reviewed herein, differences between active treatments on the primary endpoints were not dramatic. Experience in clinical practice suggests that, for many patients, oral triptans are superior to non-specific acute treatments, creating a discrepancy between clinical trials results and clinical practice experience. Four possible explanations for the disparities between clinical trials and clinical practice are likely: (i) statistically significant differences may not have emerged because the studies lack adequate statistical power; (ii) patients treated with triptans in clinical practice may be relatively more responsive to triptans and relatively less responsive to other agents than those who participate in clinical trials (patient selection); (iii) headache response at 2 h, as measured in clinical trials, may not fully capture the benefits of triptans relative to other therapies, as assessed in clinical practice; (iv) waiting until pain is moderate or severe, as required in clinical trials, may disadvantage triptans relative to comparators.

Administration, Oral↗
PubMed2004

The sumatriptan/naratriptan aggregated patient (SNAP) database: aggregation, validation and application.

Pooled data from multiple clinical trials can provide information for medical decision-making that typically cannot be derived from a single clinical trial. By increasing the sample size beyond that achievable in a single clinical trial, pooling individual-patient data from multiple trials provides additional statistical power to detect possible effects of study medication, confers the ability to detect rare outcomes, and facilitates evaluation of effects among subsets of patients. Data from pharmaceutical company-sponsored clinical trials lend themselves to data-pooling, meta-analysis, and data mining initiatives. Pharmaceutical company-sponsored clinical trials are arguably among the most rigorously designed and conducted of studies involving human subjects as a result of multidisciplinary collaboration involving clinical, academic and/or governmental investigators as well as the input and review of medical institutional bodies and regulatory authorities. This paper describes the aggregation, validation and initial analysis of data from the sumatriptan/naratriptan aggregate patient (SNAP) database, which to date comprises pooled individual-patient data from 128 clinical trials conducted from 1987 to 1998 with the migraine medications sumatriptan and naratriptan. With an extremely large sample size (>28000 migraineurs, >140000 treated migraine attacks), the SNAP database allows exploration of questions about migraine and the efficacy and safety of migraine medications that cannot be answered in single clinical trials enrolling smaller numbers of patients. Besides providing the adequate sample size to address specific questions, the SNAP database allows for subgroup analyses that are not possible in individual trial analyses due to small sample size. The SNAP database exemplifies how the wealth of data from pharmaceutical company-sponsored clinical trials can be re-used to continue to provide benefit.

Clinical Trials as Topic↗
PubMed2006

Increased expression of endothelial and neuronal nitric oxide synthase in dura and pia mater after air stress.

Stress is the leading precipitating factor for migraine attacks but the underlying mechanism is currently unknown. Nitric oxide (NO) has been implicated in migraine pathogenesis based on the ability of NO donors to induce migraine attacks. In the present study, we investigated in Wistar rats the effect of air stress on nitric oxide synthase (NOS) mRNA and protein expression in dura and pia mater using real-time polymerase chain reaction and Western blotting, respectively. Endothelial (e)NOS protein expression was significantly increased in dura and pia mater after air stress. Significantly augmented neuronal (n)NOS protein expression was detected in pia mater after air stress but not in dura mater. Inducible NOS mRNA and protein expression levels in dura and pia mater were unaffected by stress. The increased expression of eNOS in dura mater and eNOS and nNOS in pia mater seen after stress could not be antagonized by treatment with the migraine drug sumatriptan. These findings point towards the involvement of increased NO concentrations in dura and pia mater in response to air stress. However, the role of these findings in relation to migraine pathophysiology remains unclear.

Air Movements↗
PubMed1993

Release-regulating serotonin 5-HT1D autoreceptors in human cerebral cortex.

Release-regulating 5-hydroxytryptamine (5-HT) autoreceptors in the rat brain belong to the 5-HT1B subtype. On the other hand, the human brain seems to lack 5-HT1B receptors. In the present work 5-HT autoreceptors present in human brain were characterized pharmacologically. Synaptosomes prepared from biopsy samples of human neocortex were labeled with [3H]5-HT and exposed in superfusion to selective 5-HT receptor agonists and antagonists during K+ depolarization. The rank order of potency of agonists as inhibitors of the [3H]5-HT overflow was 5-HT > sumatriptan (5-HT1D/1B) > 8-hydroxy-2-(di-n-propylamino)tetralin (5-HT1A/1D) >> 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (5-HT2/1C). The effect of 5-HT was insensitive to ketanserin (5-HT2) but antagonized by methiothepin (5-HT1/2) or by metergoline (5-HT1C/1D). The data are compatible with a classification of the human 5-HT autoreceptor as being of the 5-HT1D subtype.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

CP-93,129, a potent and selective 5-HT1B receptor agonist blocks neurogenic plasma extravasation within rat but not guinea-pig dura mater.

Pretreatment with CP-93,129 blocked plasma extravasation in rat dura mater induced by electrical trigeminal ganglion stimulation when administered at greater than or equal to 140 nmol kg-1, i.v. but did not affect plasma leakage in guinea-pig at 460 or 1400 nmol kg-1. Sumatriptan, a 5-HT1D-like receptor agonist, blocked plasma extravasation in the guinea-pig model when administered at 7 nmol kg-1. In as much as CP-93,129 binds with micromolar affinities to 5-HT1A, 5-HT1C, 5-HT1D, and 5-HT2 recognition sites, and with nanomolar affinity to the 5-HT1B receptor subtype, blockade of plasma extravasation in the rat dura mater may be mediated by 5-HT1B receptors whereas the 5-HT1D receptor may be more relevant to the guinea-pig.

Animals↗
PubMed1991

Carotid vascular effects of ergotamine and dihydroergotamine in the pig: no exclusive mediation via 5-HT1-like receptors.

1. Though it is well known that the antimigraine drugs ergotamine and dihydroergotamine reduce carotid arteriovenous anastomotic shunting, it is uncertain whether a 5-HT1-like receptor is responsible for this effect. Using a high dose of methiothepin (3 mg kg-1), which completely blocks the carotid vascular effects of sumatriptan, we have attempted to study the role of 5-HT1-like receptors in the carotid vascular effects of ergotamine as well as dihydroergotamine in anaesthetized pigs. 2. Both ergotamine and dihydroergotamine increased arterial blood pressure and decreased heart rate. 3. The ergot alkaloids reduced dose-dependently total carotid blood flow and conductance as a result of a selective decrease in the arteriovenous anastomotic fraction. The nutrient fraction increased, particularly to bones, tongue and salivary glands with ergotamine and to ears, head skin, bones and salivary glands with dihydroergotamine. In contrast, dural vascular conductance tended to decrease. 4. Methiothepin (3 mg kg-1) partially antagonized the decrease in total carotid and arteriovenous anastomotic blood flow and conductance by the ergot alkaloids; the ED30 for ergotamine and dihydroergotamine (agonist dose eliciting a 30% decrease in arteriovenous anastomotic conductance) was raised by 3.1 and 5.2 fold respectively. 5. These results indicate that the effects of ergotamine and dihydroergotamine are partly mediated by methiothepin-sensitive receptors, which may probably belong to either 5-HT1-like or alpha 2-adrenoceptor category. However, an important part of the effect of ergot alkaloids is left after methiothepin and this could be mediated by other, perhaps novel, receptors.

Animals↗
PubMed1996

Functional characterization of the 5-HT terminal autoreceptor in the guinea-pig brain cortex.

1 In guinea-pig cerebral cortical slices in vitro we have shown that the rank order of potency of 5-hydroxytrptamine (5-HT), 5-carboxamidotryptamine and sumatriptan for inhibition of electrically stimulated [3H]-5-HT release correlates well with published data on their 5-HT1D receptor binding affinities. 2 Both the non-selective 5-HT1D receptor antagonist, methiothepin and the selective 5-HT1D receptor antagonist, N-[4-methoxy-3-(4-methyl-1-piperazinyl]phenyl]-2'-methyl-4'- (5-methyl-1,2,4-oxadiazole-3-yl) [1,1-biphenyl]4-carboxamide (GR127935) increased stimulated [3H]-5-HT release per se and also attenuated agonist-induced inhibition of [3H]-5-HT release. GR127935 (10 nM-100 nM) produced a pA2 of 9.0 against 5-HT, which is consistent with its 5-HT1D receptor binding affinity. 3 From these findings we conclude that, in guinea-pig cerebral cortex, the 5-HT terminal autoreceptor is of the 5-HT1D receptor subtype. However, three observations suggest the presence of multiple terminal autoreceptors: shallow inhibition curves to the agonists; a shallow Schild slope of GR127935 antagonism and differences in the maximal responses to 5-HT between whole cortex and frontal cortex.

Animals↗
PubMed1996

Influence of the endothelium and nitric oxide on the contractile responses evoked by 5-HT1D receptor agonists in the rabbit isolated saphenous vein.

1. We investigated whether contractile responses evoked by 5-HT1D receptor agonists were influenced by the endothelium (E) and nitric oxide (NO) in the rabbit isolated saphenous vein. 2. Saphenous vein rings were set up for isometric tension recording in oxygenated (5% CO2 in O2) Krebs solution (pH 7.4) containing (10(-6) M): idazoxan (1), indomethacin (10), ketanserin (0.1), prazosin (10), and N(omega) nitro-L-arginine methyl ester (L-NAME; 0 or 10), a NO synthase inhibitor. In some experiments, the E was removed mechanically. 3. 5-Hydroxytryptamine (5-HT), 5-carboxamidotryptamine (5-CT) and sumatriptan (Sum) contracted rabbit saphenous vein rings in the potency order (pD2 range) of 5-CT(7.2-7.6) > 5-HT(6.2-7.1) > Sum(5.0-5.8), irrespective of the presence or absence of the E or L-NAME (n = 9-37 per group) indicating that the potencies of the 3 agonists were not significantly affected by either the E or L-NAME. 4. Efficacy, as assessed by the maximal contractile response (Emax), was significantly greater for Sum compared to 5-HT and 5-CT with intact E irrespective of the presence (77 +/- 3, 62 +/- 3, and 50 +/- 3 mN respectively; P < 0.05 Sum versus 5-HT and 5-CT) or absence (26 +/- 3, 14 +/- 4, and 13 +/- 2 mN respectively; P < 0.05 Sum versus 5-HT and 5-CT) of L-NAME. In E-denuded rings, the Emax values were all higher than in E-intact rings and did not differ between the 3 agonists (36 +/- 4, 37 +/- 4, and 36 +/- 5 mN for Sum, 5-HT and 5-CT, respectively; P > 0.5 between the 3 agonists) indicating that an endothelium-derived relaxing factor (EDRF) counteracted the constrictor activities of the 5-HT1D receptor agonists and raising the possibility that a component of the Sum-induced contractile responses was E-dependent. Without E, the presence of L-NAME did not significantly affect the Emax values of the 3 agonists (41 +/- 4, 41 +/- 5, and 41 +/- 4 mN for Sum, 5-HT, and 5-CT respectively; P > 0.5 between the 3 agonists) indicating that the NO synthase inhibited was of endothelial origin. 5. Potentiation of the Emax of the 3 agonists by L-NAME was significantly albeit partially reversed by L-arginine (10(-2) M) indicating that NO synthase was indeed inhibited by L-NAME. Furthermore, in the presence of E, potentiation of Emax of the 3 agonists by L-NAME was mimicked by methylene blue (10(-5) M) providing further evidence that NO was involved in the attenuation by the E of the contractile responses induced by the 5-HT1D receptor agonists. 6. In the presence of an intact E and L-NAME, contractile responses elicited by 5-HT and Sum were competitively antagonized by the non-selective 5-HT1D receptor antagonist, methiothepin (pA2: 9.4 and 8.8; slopes: 0.66 and 0.81, respectively) and the highly selective 5-HT1D receptor antagonist, GR 127935 (pA2: 9.0 in each case; slopes: 1.04 and 0.93, respectively) indicating that contractions were mediated through activation of a single population of 5-HT1D receptors. Contractile responses elicited by 5-CT were also competitively antagonized by methiothepin and GR 127935, but non parallel rightward shifts of the concentration-response curves were observed suggestive of the involvement of additional but as yet unidentified receptors in mediating the 5-CT-induced responses. 7. In conclusion, the efficacy, but not the potency, of 5-HT, 5-CT and Sum in evoking 5-HT1D receptor-mediated contractile responses are subject to a substantial inhibitory influence of the E and of an EDRF (probably NO).

Animals↗
PubMed1990

The pharmacology of current anti-migraine drugs.

The major finding of this analysis is that acute anti-migraine agents (e.g., ergots, sumatriptan) share high affinity for 5-HT1D receptors. This receptor appears to be present in certain intracranial blood vessels. It is also found on nerve terminals where it inhibits the release of 5-HT and other neurotransmitters. Theoretically, 5-HT1D receptor agonists may acutely inhibit the release of vasoactive and/or pain-inducing substances in the perivascular space. Conceivably, drugs acting at this receptor would stop the progression of this perivascular process. In contrast, a number of prophylactic anti-migraine drugs share a relatively high affinity for 5-HT2 receptors in human brain. Although this receptor is also found in certain blood vessels, it is present throughout the nervous system. The receptor appears to mediate neuronal depolarizations at the cellular level. No hypothesis, at present, readily explains the effectiveness of prophylactic anti-migraine drugs based on this receptor. These data offer a novel approach to the analysis of anti-migraine agents. Drugs could be selected for use in clinical migraine studies based on their selectivity for a specific 5-HT receptor subtype. "Pure" drugs could be chosen which would essentially limit the number of possible sites of action for the drugs. For example, an agent which displays both high affinity and selectivity for 5-HT1D receptors could be clinically evaluated. Its effectiveness, or lack thereof, would indicate the importance of the specific 5-HT receptor site in the pathogenesis of migraine. Further attempts to determine a common mechanism of action for effective anti-migraine agents should facilitate the elucidation of the pathogenesis of this neurological syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1991

5-Hydroxtryptamine1D receptor agonism predicts antimigraine efficacy.

The interactions of four abortive anti-migraine agents and four prophylactic anti-migraine agents with 5-HT1D receptors in bovine brain were analyzed using radioligand binding techniques and adenylate cyclase assays. In bovine caudate, the affinities of abortive anti-migraine agents (i.e. 5-hydroxytryptamine, ergotamine, dihydroergotamine, sumatriptan) for 5-HT1D receptors range from 4.0-34 nM while the affinities of prophylactic anti-migraine agents (i.e. methysergide, amitriptyline, (-)propranolol, verapamil) range from 46-11,000 nM. In adenylate cyclase studies in bovine substantia nigra, all four abortive anti-migraine agents dose-dependently inhibit forskolin-stimulated adenylate cyclase activity, a biochemical effect mediated by 5-HT1D receptors. No agonist effect on cyclase activity is observed with the four prophylactic anti-migraine agents. These data support the hypothesis that abortive anti-migraine agents are 5-HT1D receptor agonists and that this effect may underlie their anti-migraine efficacy.

Adenylyl Cyclase Inhibitors↗
PubMedDate not supplied

Wolff Award presentation 1993. Anti-migraine drug interactions with cloned human 5-hydroxytryptamine1 receptor subtypes.

Multiple 5-hydroxytryptamine (5-HT) receptors have been identified in humans. A subgroup of these receptors (designated 5-HT1 receptors) have been hypothesized to be involved in the mechanism of action of acute anti-migraine drugs. At present, this hypothesis cannot be tested directly in human tissues due to technical limitations. However, recent molecular biological advances have allowed for the development of assays employing cloned human 5-HT1 receptors expressed in cells by DNA transfection. This study analyzed the ability of ergotamine, dihydroergotamine, and 5-HT and sumatriptan to interact with the four known human 5-HT1 receptor subtypes. The four acute anti-migraine agents interacted with all 4 human 5-HT1 receptor subtypes with less than 1 microM affinity. However, drug affinities for the human 5-HT1B and 5-HT1D receptors correlate most closely with the rank order of clinical dosages used to treat a migraine attack. Therefore, these data indicate that human 5-HT1B and/or 5-HT1D receptors are likely to mediate the therapeutic efficacy of acute anti-migraine drugs.

Ergotamine↗
PubMed1994

Migraine treatment: the British perspective.

Migraine occurs in about 10% of the population in the United States and the United Kingdom. In the United States there seem to be more complicated patients and the expectations of the patient are higher. In the United Kingdom there is a tendency to use single rather than compound formulations, and drugs such as barbiturates cannot be prescribed for migraine. In treating migraine the first and most important thing is to get the correct diagnosis which depends on the history and the absence of abnormal physical signs. Investigations do not confirm the diagnosis of migraine, they are only necessary to exclude other causes of headaches. Most sufferers from migraine have less than four attacks a month. Attack therapy is usually all that is required, and over the past 20 years efficient attack therapy has been developed. This depends mainly on sleep, an antinauseant, analgesics, ergotamine and more recently sumatriptan.

Acute Disease↗
PubMed2005

Correlation between lipophilicity and triptan outcomes.

BACKGROUND: It has been suggested that triptans achieving higher central nervous system (CNS) levels should have an advantage in efficacy, if central actions are important. Objective.-Our aim was to correlate the efficacy and tolerability results of triptans with their lipophilicity. METHODS: Data for response and pain free at 2 hours, recurrence, adverse events (AE), CNS AE, and chest symptoms taken from Ferrari et al's meta-analysis publications for the recommended doses of oral triptans were correlated with their lipophilicity coefficients (logD(pH)7.4 = -2.1 almotriptan < -1.5 sumatriptan < -1.0 zolmitriptan < -0.7 rizatriptan < -0.2 naratriptan < 0.5 eletriptan). RESULTS: We found no significant correlation between lipophilicity coefficients and any of the analyzed parameters. There was, however, some correlation between lipophilicity and CNS AE (P = .09, r = 0.74) and, to a lesser degree, with a reduction in recurrence rate (r = -0.36). The r values for response and pain free with placebo correction ranged from 0.04 to 0.34, suggesting almost no correlation between lipophilicity and efficacy variables. CONCLUSIONS: According to this analysis, a higher lipophilicity does not seem crucial to improve triptan efficacy. This physico-chemical property, however, correlates with higher CNS AE and, possibly, lower recurrence rates.

Central Nervous System Diseases↗
PubMed2006

Salivary levels of CGRP and VIP in rhinosinusitis and migraine patients.

BACKGROUND: Secretion of calcitonin gene-related peptide (CGRP) from trigeminal nerves and vasoactive intestinal peptide (VIP) from parasympathetic nerves is involved in the pathophysiology of migraine and rhinosinusitis. Analysis of these neuropeptides in human saliva samples can be used as markers of trigeminal and parasympathetic nerve activity in patients between and during attacks as well as in response to specific treatments. OBJECTIVE: To compare the amount of trigeminal sensory and parasympathetic nerve activation by measuring CGRP and VIP levels in the saliva of subjects experiencing noninfectious allergic rhinosinusitis, migraine with sinus symptoms, and no symptoms. METHODS: Subjects were enrolled in three groups. Group A: subjects without a history of migraine, "sinus" headache, or allergic rhinosinusitis within the previous 6 months. Group B: subjects with chronic recurrent noninfectious rhinosinusitis and no history of migraine or "sinus" headache. Group C: subjects with self-described "sinus" headaches whose symptoms met International Headache Society diagnostic criteria (1.1 or 1.2) for migraine. The total amount of CGRP and VIP present in saliva collected under normal, pathological, and therapeutic conditions was determined by radioimmunoassay. Neuropeptide levels were normalized to total volume and amount of protein, and levels were correlated to onset and change in clinical symptoms. RESULTS: Total volume, total protein, and CGRP and VIP levels did not significantly change in saliva collected on consecutive days in the clinic and at the subject's home, respectively. No appreciable change in baseline salivary levels of CGRP and VIP was detected in control subjects. However, baseline salivary levels of CGRP and VIP were significantly elevated between attacks in allergic rhinosinusitis and migraine subjects compared to control values. For rhinosinusitis subjects, the amount of CGRP and VIP during attacks returned to baseline values following treatment with pseudoephedrine and relief of symptoms. Similarly, CGRP and VIP levels during a migraine headache were significantly reduced within 2 hours after sumatriptan treatment and reported symptom relief. CONCLUSION: Correlation of CGRP and VIP saliva levels observed in our study supports physiologically coordinated regulation of trigeminal and parasympathetic nerve activation in allergic rhinosinusitis and migraine patients between and during attacks as well as following treatment. Furthermore, our findings demonstrate that analysis of human saliva neuropeptides may provide a semiquantitative index of pathological and therapeutic states and, therefore, function as a clinical model for studying neuronal mechanisms involved in migraine and rhinosinusitis.

Adolescent↗
PubMed2006

Cluster headache: clinical presentation, lifestyle features, and medical treatment.

BACKGROUND: Cluster headache (CH) is a rare but severe headache form with a distinct clinical presentation. Misdiagnoses and mismanagement among these patients are high. OBJECTIVE: To characterize clinical features and medical treatment in patients with CH. METHODS: We established a cohort of 246 clinic-based and non-clinic-based CH patients. The diagnosis of CH was verified according to International Headache Society (IHS) criteria. We used standardized questionnaires to assess associated factors as well as success or failure of treatments. RESULTS: The majority (75.6%) was not treated before at our clinic-77.6% were males; 74.8% had episodic CH, 16.7% had chronic CH, in the remaining patients, the periodicity was undetermined because they were newly diagnosed. Cranial autonomic features were present in 98.8%, nausea and vomiting in 27.8%, and photophobia or phonophobia in 61.2% of CH patients. Most (67.9%) reported restlessness during attacks and 23% a typical migrainous aura preceding the attacks. The rate of current smoking was high (65.9%). Half of the patients reported that alcohol (red wine in 70%) triggered CH attacks. Eighty-seven percent reported the use of drugs of first choice (triptans 77.6%, oxygen 71.1%) with sumatriptan subcutaneous injection being the most effective drug for acute therapy (81.2%). The most frequently used preventive medications were verapamil (70.3%) and glucocorticoids (57.7%) with equally high effectiveness. CONCLUSIONS: Apart from the IHS criteria additional features like nausea/vomiting and migrainous aura may guide the diagnosis of CH. A large number of CH patients do not receive adequate treatments.

Adult↗