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Migraine Headache (migraine + headache)

Distribution by Scientific Domains

Medical Sciences	96%

Selected Abstracts

Divalproex Sodium Extended-Release for the Prophylaxis of Migraine Headache in Adolescents: Results of a Stand-Alone, Long-Term Open-Label Safety Study

HEADACHE, Issue 1 2009
George Apostol MD
Objective., The objective of this long-term open-label study in adolescents was to assess the safety and tolerability of divalproex sodium extended-release in the prophylaxis of migraine headaches. Background., Two formulations of divalproex sodium have demonstrated efficacy in the prevention of migraine headaches in adults. However, no medications are currently approved for this indication in adolescents, and long-term safety data on agents for migraine prevention are lacking for this younger population. Therefore, the current study was conducted to assess the long-term safety and tolerability of divalproex extended-release in adolescents with migraine headaches. Methods., This was a 12-month, phase 3, open-label, multicenter study of adolescents aged 12 to 17 years with migraine headaches diagnosed by International Headache Society criteria. Divalproex sodium extended-release was initiated at 500 mg/day for 15 days then increased to 1000 mg daily, with subsequent adjustments permitted within a dosing range of 250-1000 mg daily. Study visits were conducted at days 1 and 15 and months 1, 2, 3, 6, 9, and 12. Safety was evaluated by adverse event collection, laboratory assessments, physical and neurological examinations, vital signs, electrocardiograms, the Udvalg for Kliniske Undersøgelser Side Effect Rating Scale, the Wechsler Abbreviated Scale of Intelligence, and the Behavioral Assessment Scale for Children. Efficacy was evaluated by following the number of migraine headache days reported in subjects' headache diaries over sequential 4-week intervals for the duration of the trial. Results., A total of 241 subjects were enrolled and treated. The most frequently reported adverse events were nausea (19%), vomiting (18%), weight gain (12%), nasopharyngitis (11%), migraine (10%), and upper respiratory tract infection (10%). Ten (4%) subjects experienced serious adverse events, and 40 (17%) subjects discontinued because of an adverse event. Increases in ammonia levels were observed. No other clinically significant changes were observed in laboratory values, vital signs, rating scales, or electrocardiograms. Median 4-week migraine headache days decreased 75% between the first and the fourth months of the study (from 4.0 to 1.0) and remained at or below this level for the remainder of the study. Conclusions., In this long-term open-label study of adolescents with migraine, the safety and tolerability profile of divalproex sodium extended-release was consistent with findings from previous trials in adults, as well as 2 studies recently completed in adolescents. In general, divalproex sodium extended-release was well-tolerated in adolescents with migraine. [source]

Ovarian Hormones and Migraine Headache: Understanding Mechanisms and Pathogenesis,Part 2

HEADACHE, Issue 3 2006
Vincent T. Martin MD
Migraine headache is strongly influenced by reproductive events that occur throughout the lifespan of women. Each of these reproductive events has a different "hormonal milieu," which might modulate the clinical course of migraine headache. Estrogen and progesterone can be preventative or provocative for migraine headache under different circumstances depending on their absolute serum levels, constancy of exposure, and types of estrogen/progesterone derivatives. Attacks of migraine with and without aura respond differently to changes in ovarian hormones. Clearly a greater knowledge of ovarian hormones and their effect on migraine is essential to a greater understanding of the mechanisms and pathogenesis of migraine headache. [source]

Carnitine Palmityltransferase II (CPT2) Deficiency and Migraine Headache: Two Case Reports

HEADACHE, Issue 5 2003
Marielle A. Kabbouche MD
Background.,Migraine headache is common and has multiple etiologies. A number of mitochondrial anomalies have been described for migraine, and mitochondrial dysfunction has been implicated as one potential pathophysiological mechanism. Carnitine is used by mitochondria for fatty acid transportation; its deficiency, however, has not been implicated in migraine pathophysiology. Methods and Results.,Two adolescent girls presented to the Headache Center at Cincinnati Children's Hospital Medical Center with frequent headaches and were diagnosed with migraine by the International Headache Society (IHS) criteria. Both girls had a history of recurrent fatigue, muscle cramps, and multiple side effects from their prophylactic treatment. Carnitine levels were measured and found to be low. Carnitine supplementation was initiated. Both patients had a reduction in headache frequency, as well as an improvement in their associated symptoms and other complaints. A skin and muscle biopsy obtained from one patient revealed a partial carnitine palmityltransferase II deficiency in the muscle only. Conclusion.,Carnitine palmityltransferase II deficiency may represent another etiology for migraine headache, and may be useful in further defining the pathophysiology of migraine. When properly recognized, supplementation with carnitine may improve the outcome of the migraine as well as the carnitine-associated symptoms. [source]

Biofeedback-Assisted Relaxation in Migraine Headache: Relationship to Cerebral Blood Flow Velocity in the Middle Cerebral Artery

HEADACHE, Issue 3 2003
Sachinder Vasudeva MD
Objective.,To determine if migraineurs with aura respond differently to biofeedback/relaxation than those without aura and, if so, whether the variability in outcome can be explained by blood flow velocity. Background.,The relationship between cerebral blood flow velocity and treatment response to biofeedback/relaxation in migraine with and without aura is uncertain. Method.,Twenty migraineurs underwent 12 sessions of biofeedback/relaxation therapy, while 20 controls simply were told to relax on their own. Cerebral blood flow velocity was measured bilaterally in the middle cerebral artery with transcranial Doppler. Results.,The biofeedback group showed significant (P < .05) reductions in pain, depression, and anxiety compared to the control group. Patients with and without aura did equally well. There were significant (P < .05) left to right blood flow velocity differences only in the migraine with aura group. Maximum blood flow velocities were significantly higher (P < .05) in the migraine with aura group than in the cohort without aura. There was an inverse correlation between indicators of anxiety and blood flow velocity, perhaps related to hyperventilation-induced constriction in the small vessels distal to the middle cerebral artery. Conclusion.,The positive treatment response to biofeedback/relaxation in migraine headache is not related to presence of aura, nor to changes in blood flow velocity, but may be associated with reduction in anxiety and depression. [source]

Does the Addition of Dexamethasone to Standard Therapy for Acute Migraine Headache Decrease the Incidence of Recurrent Headache for Patients Treated in the Emergency Department?

ACADEMIC EMERGENCY MEDICINE, Issue 12 2008
A Meta-analysis, Systematic Review of the Literature
Abstract Objectives:, Neurogenic inflammation is thought to play a role in the development and perpetuation of migraine headache. The emergency department (ED) administration of dexamethasone in addition to standard antimigraine therapy has been used to decrease the incidence of recurrent headaches at 24 to 72 hours following evaluation. This systematic review details the completed trials that have evaluated the use of dexamethasone in this role. Methods:, The authors searched MEDLINE, EMBASE, CINAHL, LILACS, recent emergency medicine scientific abstracts, and several prepublication trial registries for potential investigations related to the research question. The authors included studies that incorporated randomized, double-blind, placebo-controlled methodology and that were performed in the ED. A fixed-effects and random-effects model was used to obtain summary risk ratios (RRs) and 95% confidence intervals (CIs) for the self-reported outcome of moderate or severe headache on follow-up evaluation. Results:, A pooled analysis of seven trials involving 742 patients suggests a modest but significant benefit when dexamethasone is added to standard antimigraine therapy to reduce the rate of patients with moderate or severe headache on 24- to 72-hour follow-up evaluation (RR = 0.87, 95% CI = 0.80 to 0.95; absolute risk reduction = 9.7%). The treatment of 1,000 patients with acute migraine headache using dexamethasone in addition to standard antimigraine therapy would be expected to prevent 97 patients from experiencing the outcome of moderate or severe headache at 24 to 72 hours after ED evaluation. The sensitivity analysis yielded similar results with sequential trial elimination, indicating that no single trial was responsible for the overall result. Adverse effects related to the administration of a single dose of dexamethasone were infrequent, mild, and transient. Conclusions:, These results suggest that dexamethasone is efficacious in preventing headache recurrence and safe when added to standard treatment for the management of acute migraine headache in the ED. [source]

From Migraine To Chronic Daily Headache: The Biological Basis of Headache Transformation

HEADACHE, Issue 8 2007
Ian D. Meng PhD
Migraine headache carries the potential of transforming into chronic daily headache (CDH) over a period of time. Although several risk factors for migraine progression to CDH have been identified, the biological basis of this transformation is unknown. In this review, the consequences of stressful life events and medication overuse, 2 risk factors associated with the development of CDH, on brain processes involved in headache are examined. The extensive overlap in both neural circuitry and cellular events that occur with stress, medication overuse, and migraine provide insight into potential mechanisms that may lead to CDH. Particular attention is devoted to the effect of stress and medication overuse on peripheral and central neuroimmune interactions that can facilitate pain signaling. These interactions include the degranulation of mast cells in the dura, causing the sensitization of primary afferent neurons, as well as the activation of glial cells in the brain that can lead to central sensitization. It is hypothesized that the biological processes involved in migraine headache are directly impacted by stress, medication overuse, and other risk factors, resulting in a reduced threshold for induction of headache and transformation of episodic migraine to CDH. [source]

Ovarian Hormones and Migraine Headache: Understanding Mechanisms and Pathogenesis,Part 2

Carnitine Palmityltransferase II (CPT2) Deficiency and Migraine Headache: Two Case Reports

Sensitization of meningeal nociceptors: inhibition by naproxen

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2008
Dan Levy
Abstract Migraine attacks associated with throbbing (manifestation of peripheral sensitization) and cutaneous allodynia (manifestation of central sensitization) are readily terminated by intravenous administration of a non-selective cyclooxygenase (COX) inhibitor. Evidence that sensitization of rat central trigeminovascular neurons was also terminated in vivo by non-selective COX inhibition has led us to propose that COX inhibitors may act centrally in the dorsal horn. In the present study, we examined whether COX inhibition can also suppress peripheral sensitization in meningeal nociceptors. Using single-unit recording in the trigeminal ganglion in vivo, we found that intravenous infusion of naproxen, a non-selective COX inhibitor, reversed measures of sensitization induced in meningeal nociceptors by prior exposure of the dura to inflammatory soup (IS): ongoing activity of A,- and C-units and their response magnitude to mechanical stimulation of the dura, which were enhanced after IS, returned to baseline after naproxen infusion. Topical application of naproxen or the selective COX-2 inhibitor N -[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS-398) onto the dural receptive field of A,- and C-unit nociceptors also reversed the neuronal hyper-responsiveness to mechanical stimulation of the dura. The findings suggest that local COX activity in the dura could mediate the peripheral sensitization that underlies migraine headache. [source]

Long-Term, Open-Label Safety Study of Oral Almotriptan 12.5 mg for the Acute Treatment of Migraine in Adolescents

HEADACHE, Issue 5 2010
Frank Berenson MD
(Headache 2010;50:795-807) Objectives., This study evaluated the long-term safety of oral almotriptan 12.5 mg for the treatment of multiple migraine episodes in adolescents over a 12-month period. Efficacy outcomes were assessed as a secondary objective. Methods., Adolescent migraineurs aged 12-17 years were enrolled in this 12-month, open-label study (Study ID CR002827). Patients were instructed to record their assessments on paper headache records whenever they experienced a migraine headache that they treated with study medication. Safety was assessed descriptively and assessments included adverse event (AE) recording, change in laboratory values, vital signs, and electrocardiogram parameters. Efficacy outcomes were assessed descriptively and outcomes included rates for 2- and 24-hour pain relief and sustained pain relief, 2- and 24-hour pain-free and sustained pain-free, and presence of migraine-associated symptoms of photophobia, phonophobia, nausea and vomiting. Results., Overall, 67.1% of patients reported ,1 AE over the course of the trial, 7.6% had an AE judged by the study investigator to be related to treatment with almotriptan, 2.4% discontinued because of an AE, and 1.9% reported serious AEs. The most commonly reported treatment-related AEs (occurring in ,1% of patients) were nausea (1.4%) and somnolence (1.4%). Pain relief responses for treated migraines of moderate or severe intensity at baseline were 61.7% and 68.6%, at 2 and 24 hours, respectively; the sustained pain relief rate was 55.5%. Pain-free responses were reported for 40.5% of all treated migraines at 2 hours and 65.9% of treated migraines at 24 hours; the sustained pain-free rate was 38.4%. The proportion of migraines that achieved the pain relief, sustained pain relief, pain-free and sustained pain-free endpoints were similar in the 12- to 14-year and 15- to 17-year age groups. Treating with almotriptan 12.5 mg when headache pain was mild was associated with higher rates of pain relief and pain-free at 2 and 24 hours, and sustained pain relief and sustained pain-free, compared with treatment initiated when pain was severe. Conclusions., Almotriptan 12.5 mg was well tolerated in this adolescent population over a 12-month period. No unexpected safety or tolerability concerns were revealed over the course of this study. The results are consistent with almotriptan 12.5 mg being effective for the acute treatment of pain and symptoms associated with migraine in both younger and older adolescents. [source]

Migraine Pain and Nociceptor Activation,Where Do We Stand?

HEADACHE, Issue 5 2010
Dan Levy PhD
The mechanisms underlying the genesis of migraine pain remain enigmatic largely because of the absence of any identifiable cephalic pathology. Based on numerous indirect lines of evidence, 2 nonmutually exclusive hypotheses have been put forward. The first theorizes that migraine pain originates in the periphery and requires the activation of primary afferent nociceptive neurons that innervate cephalic tissues, primarily the cranial meninges and their related blood vessels. The second maintains that nociceptor activation may not be required and that the headache is promoted primarily as a result of abnormal processing of sensory signals in the central nervous system. This paper reviews the evidence leading to these disparate theories while siding with the primacy of nociceptor activation in the genesis migraine headache. The paper further examines the potential future use of established human models of migraine for addressing the origin of migraine headache. [source]

Posterior Ischemic Optic Neuropathy Associated With Migraine

HEADACHE, Issue 7 2008
Rod Foroozan MD
Posterior ischemic optic neuropathy (PION) is an uncommon form of optic nerve ischemia that results from damage to the intraorbital, intracanalicular, or intracranial optic nerve. It has been reported perioperatively, in association with systemic vasculitis, and in the nonsurgical setting with no identifiable cause. Review of the literature reveals only 2 patients with PION associated with migraine in a single report. We report a patient who developed PION in the setting of a migraine headache without any other identifiable risk factors. [source]

A Pivotal Moment in 50 Years of Headache History: The First American Migraine Study

HEADACHE, Issue 5 2008
Stewart J. Tepper MD
Objective., To describe the magnitude and distribution of the public health problem posed by migraine in the United States by examining migraine prevalence, attack frequency, and attack-related disability by gender, age, race, household income, geographic region, and urban vs rural residence. Design., In 1989, a self-administered questionnaire was sent to a sample of 15,000 households. A designated member of each household initially responded to the questionnaire. Each household member with severe headache was asked to respond to detailed questions about symptoms, frequency, and severity of headaches. Setting., A sample of households selected from a panel to be representative of the US population in terms of age, gender, household size, and geographic area. Participants., After a single mailing, 20,468 subjects (63.4% response rate) between 12 and 80 Years of age responded to the survey. Respondents and nonrespondents did not differ by gender, household income, region of the country, or urban vs rural status. Whites and the elderly were more likely to respond. Migraine headache cases were identified on the basis of reported symptoms using established diagnostic criteria. Results., In total, 17.6% of females and 5.7% of males were found to have 1 or more migraine headaches per year. The prevalence of migraine varied considerably by age and was highest in both men and women between the ages of 35 to 45 years. Migraine prevalence was strongly associated with household income; prevalence in the lowest-income group (less than $10,000) was more than 60% higher than in the 2 highest-income groups (greater than or equal to $30,000). The proportion of migraine sufferers who experienced moderate to severe disability was not related to gender, age, income, urban vs rural residence, or region of the country. In contrast, the frequency of headaches was lower in higher-income groups. Attack frequency was inversely related to disability. Conclusions., A projection to the US population suggests that 8.7 million females and 2.6 million males suffer from migraine headache with moderate to severe disability. Of these, 3.4 million females and 1.1 million males experience 1 or more attacks per month. Females between ages 30 and 49 years from lower-income households are at especially high risk of having migraines and are more likely than other groups to use emergency care services for their acute condition. [source]

Neuromodulators for Migraine Prevention

HEADACHE, Issue 4 2008
Robert Kaniecki MD
Migraine is a debilitating condition characterized by a cycle of painful headaches and headache-related symptoms interspersed with periods of worry, distress, and apprehension. The negative impact of migraine on patient functioning, workplace productivity, and other daily activities has been demonstrated through the use of a variety of clinician- and patient-reported assessment tools, including the Migraine-Specific Questionnaire and the Migraine Disability Assessment questionnaire. In addition to considering the frequency and severity of migraine, clinicians need to encourage more open dialogue with their patients about the impact of this disorder on daily activities and productivity. Only then can the most appropriate course of treatment be determined. Appropriately prescribed acute and preventive therapies should break the cycle of migraine and improve the daily activities of patients with this chronic condition. Divalproex sodium and topiramate are neuromodulators that are approved by the US Food and Drug Administration (FDA) for the prophylaxis (prevention) of migraine headache in adults. Non-FDA-approved neuromodulators sometimes used in the management of migraine headache include gabapentin, lamotrigine, levetiracetam, and zonisamide. All medications need to be titrated, and treatment-related adverse events need to be managed appropriately. Preventive medications should be taken for at least 2-3 months to ascertain their therapeutic effect. [source]

From Migraine To Chronic Daily Headache: The Biological Basis of Headache Transformation

Efficacy of Eletriptan in Migraine-Related Functional Impairment: Functional and Work Productivity Outcomes

HEADACHE, Issue 5 2007
Stephen D. Silberstein MD
Objective.,To provide a multidimensional assessment of the extent of functional impairment during an acute migraine attack, and of the improvement in functioning in response to treatment, using 4 concurrently administered scales: the 7-item work productivity questionnaire (PQ-7), the functional assessment in migraine (FAIM) activities and participation (FAIM-A&P) subscale, the FAIM-impact of migraine on mental functioning (FAIM-IMMF) subscale, and the traditional 4-point global functional impairment scale (FIS). Methods.,Outpatients with an International Classification of Headache Disorders diagnosis of migraine were randomized to double-blind treatment of a single attack with either oral eletriptan 20 mg (n = 192) once-daily, eletriptan 40 mg (N = 213) once-daily, or placebo (n = 208). Patients were encouraged to take study medication as soon as they were sure they were experiencing a typical migraine headache, after the aura phase (if present) had ended. Patients with moderate-to-severe functional impairment were identified on each of the 4 disability scales, and 2-hour functional response was compared between treatments. Results.,At baseline, the PQ-7 and FAIM-IMMF items that assessed ability to perform tasks requiring concentration, sustained work or attention, and ability to think quickly or spontaneously, were especially sensitive to the effects of mild headache pain, with 27% to 48% of patients (n = 92-112) reporting moderate-to-severe impairment. Only 11.3% of patients (n = 112) reported this level of impairment due to mild pain on the FIS. Functional response at 2 hours was significantly higher on eletriptan 40 mg versus placebo on the FAIM-A&P (63% vs 36%; n = 218; P < .0001); on the PQ-7 (56% vs 34%; n = 116; P= .0052); and on the FAIM-IMMF (50% vs 34%; n = 215; P= .017). These rates were all lower than the functional response rates on the FIS for eletriptan 40 mg (75%) and eletriptan 20 mg (70%) versus placebo (45%; P < .001). Conclusions.,In this exploratory analysis, use of multidimensional scales was found to provide a sensitive measure of headache-related functional impairment, especially for detecting clinically meaningful cognitive effects, and for detecting drug versus placebo differences. [source]

Ovarian Hormones and Migraine Headache: Understanding Mechanisms and Pathogenesis,Part 2

Migraine Treatment With Rizatriptan and Non-Triptan Usual Care Medications: A Pharmacy-Based Study

HEADACHE, Issue 9 2004
Roger Cady MD
Objective.,To compare the effectiveness of rizatriptan to other non-triptan medications in the relief of migraine headache in usual care settings. Background.,Although rizatriptan has been shown to provide effective relief of migraine symptoms in clinical trials, limited data exist directly comparing its effectiveness with non-triptan medications. Methods.,Migraineurs aged 18 to 55 who had been prescribed a new antimigraine drug (rizatriptan 10 mg or a selected class of non-triptan oral medications) were recruited to participate in the study through a national retail pharmacy chain. Participants completed a baseline questionnaire at the enrollment and reported their treatment experiences by filling out the treatment diary after using the newly prescribed medication. The treatment outcomes of patients receiving rizatriptan were compared with those receiving non-triptan medications. Logistic regression analysis was applied to test statistical significance with adjustment for potential confounding factors. Results.,Of the 728 patients who entered the study, 693 (95.2%) completed the treatment diary. Patients treated with rizatriptan (192) and non-triptans (501) reported the following outcomes, respectively,onset of headache relief within 30 minutes post-dose: 25% versus 18%; self-defined significant headache relief within 2 hours post-dose: 71% versus 54%; pain free or mild pain at 2 hours post-dose: 58% versus 47%; completely symptom-free within 2 hours of post-dose: 32% versus 20%; return to usual activities within 2 hours post-dose: 39% versus 35%; and satisfied with treatment: 67% versus 55% (P < .05 in all comparisons with exception of returning to usual activities). Conclusion.,Rizatriptan was significantly more effective than non-triptans in the relief of migraine headaches for patients obtaining prescribed migraine medications from a retail pharmacy. Additional studies at other usual care settings may be needed to confirm the findings. [source]

Carnitine Palmityltransferase II (CPT2) Deficiency and Migraine Headache: Two Case Reports

Biofeedback-Assisted Relaxation in Migraine Headache: Relationship to Cerebral Blood Flow Velocity in the Middle Cerebral Artery

Antiepileptic Drugs in Migraine Prevention

HEADACHE, Issue 2001
Ninan T. Mathew MD
Migraineurs may continue to experience attacks, despite daily use of one or more agents from a wide range of drugs, including , -blockers, calcium channel blockers, serotonin antagonists, tricyclic antidepressants, monoamine oxidase inhibitors, and antiepileptic agents. Divalproex sodium is the only antiepileptic drug approved for migraine prevention. Gabapentin, topiramate, and other antiepileptic agents are being evaluated for migraine prevention and treatment. Prospective, double-blind, placebo-controlled clinical trials of divalproex, gabapentin, and topiramate for migraine prevention generally were composed of a prospective baseline period, a dose titration period, and a fixed-dose treatment period. The primary efficacy variable was a reduction in the 28-day frequency of migraine headache. Patients receiving divalproex for 12 weeks at doses up to 1500 mg/day achieved significant decreases in the migraine frequency (P<.05), corresponding to reductions of 30% to 40% compared with baseline. Nearly half of the divalproex-treated patients had a 50% or more reduction from baseline in headache frequencies (P.05). Asthenia, vomiting, somnolence, tremor, and alopecia were common adverse events associated with divalproex. Significant reductions in migraine frequency were also observed with gabapentin (1800 to 2400 mg/day) when compared with placebo (P<.01), and nearly half of all patients treated at the highest dose experienced a reduction in headache rate of 50% or more. Somnolence was the most commonly reported adverse event among the gabapentin-treated patients. Two single-center, double-blind, placebo-controlled clinical trials evaluated topiramate for migraine prevention. A lower 28-day migraine frequency was seen during 18 weeks of administration at a maximum daily dose of 200 mg (P = .09). In a second study, a significantly lower mean 28-day migraine frequency was observed during 16 weeks of treatment with topiramate (P = .0015). Mean reduction in migraine frequency was also significantly greater in topiramate-treated patients (P = .0037). Paresthesias, diarrhea, somnolence, and altered taste were commonly reported adverse events in the topiramate-treated patients. Unlike some patients given divalproex or gabapentin, some given topiramate reported weight loss. Large, double-blind, placebo-controlled trials may prove the effectiveness of novel antiepileptic drugs in migraine prevention. [source]

Acute treatment of paediatric migraine: A meta-analysis of efficacy

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 1-2 2008
Shawna Silver
Aim: To undertake a meta-analysis of all randomised controlled trials (RCTs) on the acute pharmacologic treatment of children and adolescents with migraine headache. Methods: In total, 139 abstracts of clinical trials specific to the acute treatment of paediatric migraine were appraised. Inclusion criteria required clinical trials to be randomised, blinded, placebo-controlled studies with comparable endpoints. Non- English language publications were excluded. 11 clinical trials qualified for inclusion in the final meta-analysis. Two endpoints were analysed: the proportion of patients with (1) headache relief, and (2) complete pain relief, 2 h post-treatment. Results: The following medications were included in the analysis: acetaminophen (n = 1), ibuprofen (n = 2), sumatriptan (n = 5), zolmitriptan (n = 1), rizatriptan (n = 2) and dihydroergotamine (n = 1). Results are expressed as a relative benefit (RB) conferred over placebo and the number needed to treat (NNT). Only ibuprofen and sumatriptan provided a statistically significant relative efficacy in comparison with placebo. Two hours post-treatment, ibuprofen was associated with an RB 1.50 (95% CI 1.15,1.95) in the generation of headache relief (NNT 2.4) and RB 1.92 (95% CI 1.28,2.86) in the production of complete pain relief (NNT 4.9). Sumatriptan rendered an RB 1.26 (95% CI 1.13,1.41) in headache relief (NNT 7.4) and an RB 1.56 (95% CI 1.26,1.93) in the production of complete pain relief (NNT 6.9). Conclusion: Despite the pharmacological options for the management of acute migraine, few RCTs in the paediatric population exist. Composite data demonstrate that only ibuprofen and sumatriptan are significantly more effective than placebo in the generation of headache relief in children and adolescents. [source]

Who are the nonresponders to standard treatment with tricyclic antidepressant agents for cyclic vomiting syndrome in adults?

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2 2010
R. A. HEJAZI
Summary Background, Cyclic vomiting syndrome in adults is a disorder characterized by recurrent and stereotypic episodes of severe nausea and vomiting separated by symptom-free periods. Aims, To investigate the demographic and clinical characteristics of adult cyclic vomiting syndrome patients not responding to standard tricyclic antidepressant (TCA) therapy. Methods, A total of 132 adults (62 men) with cyclic vomiting syndrome were followed for a mean of 1.6 years. Of these, 17 (eight men) patients were identified as nonresponders based on the criteria of unchanged, increased or minimally changed (<25%) frequency/duration of episodes and/or emergency department visits/hospitalizations. Demographic and clinical characteristics at baseline and annually up to 4 years were investigated. Results, The nonresponders were receiving TCAs at an average dose of 90 mg/day compared to a mean dose of 85 mg/day in responders. Compared with the responders, the nonresponders were significantly more likely to have a history of migraine (P < 0.05); co-existing psychological disorders (P < 0.05); chronic marijuana use (P < 0.05) and reliance on narcotics for pain control between cyclic vomiting syndrome episodes (P < 0.05). Conclusions, (1) Nonresponse to standard therapy in adult cyclic vomiting syndrome patients occurs in approximately 13% and is not explained by under dosing with TCA therapy. (2) The main risk factors for nonresponse are: co-existing migraine headache, psychiatric disorder, chronic narcotic and marijuana use, which should be addressed aggressively when symptom exacerbations continue during attempts to induce remission in cyclic vomiting syndrome with high-dose TCA therapy. Aliment Pharmacol Ther,31, 295,301 [source]

Persistent Genital and Pelvic Pain after Childbirth

THE JOURNAL OF SEXUAL MEDICINE, Issue 1 2009
Laurel Q.P. Paterson BA
ABSTRACT Introduction., Although genital pain and pelvic pain are common and well-documented problems in the early postpartum period, little is known about their course. The few published studies of such pain beyond 1 year postpartum have focused primarily on the perineum and have not assessed pain onset. Aim., To investigate the prevalence and characteristics of all types of genital and pelvic pain in the second year postpartum, and to explore risk factors for their persistence. Methods., Over a 6-month period, a questionnaire on genital/pelvic pain, sociodemographic and childbirth variables, breastfeeding, and chronic pain history was mailed to patients of the collaborating obstetrician at 12 months postpartum. Main Outcome Measures., The prevalence, characteristics, and correlates of persistent genital/pelvic pain with postpartum onset. Results., Almost half of the 114 participants (82% response rate; M = 14 months postpartum) reported a current (18%) or resolved (26%) episode of genital or pelvic pain lasting 3 or more months. Just under one in 10 (9%) mothers continued to experience pain that had begun after they last gave birth. This pain was described at various locations (e.g., vaginal opening and pelvic area), as moderate in intensity and unpleasantness, and most often as burning, cutting, or radiating. Although it was triggered by both sexual and nonsexual activities, none of the mothers affected were receiving treatment. Univariate analyses revealed that only past diagnosis with a nongenital chronic pain condition (e.g., migraine headache) was significantly correlated with (i) any history of chronic genital/pelvic pain or (ii) the persistence of pregnancy- or postpartum-onset genital or pelvic pain. Conclusions., Postpartum genital and pelvic pain persists for longer than a year for a significant percentage of mothers. Women with a history of other chronic pain appear to be particularly vulnerable to developing persistent genital or pelvic pain. Paterson LQP, Davis SNP, Khalifé S, Amsel R, and Binik YM. Persistent genital and pelvic pain after childbirth. J Sex Med 2009;6:215,221. [source]

Thalamic sensitization transforms localized pain into widespread allodynia

ANNALS OF NEUROLOGY, Issue 1 2010
Rami Burstein PhD
Objective Focal somatic pain can evolve into widespread hypersensitivity to nonpainful and painful skin stimuli (allodynia and hyperalgesia, respectively). We hypothesized that transformation of headache into whole-body allodynia/hyperalgesia during a migraine attack is mediated by sensitization of thalamic neurons that process converging sensory impulses from the cranial meninges and extracephalic skin. Methods Extracephalic allodynia was assessed using single unit recording of thalamic trigeminovascular neurons in rats and contrast analysis of blood oxygenation level-dependent (BOLD) signals registered in functional magnetic resonance imaging (fMRI) scans of patients exhibiting extracephalic allodynia. Results Sensory neurons in the rat posterior thalamus that were activated and sensitized by chemical stimulation of the cranial dura exhibited long-lasting hyperexcitability to innocuous (brush, pressure) and noxious (pinch, heat) stimulation of the paws. Innocuous, extracephalic skin stimuli that did not produce neuronal firing at baseline (eg, brush) became as effective as noxious stimuli (eg, pinch) in eliciting large bouts of neuronal firing after sensitization was established. In migraine patients, fMRI assessment of BOLD signals showed that brush and heat stimulation at the skin of the dorsum of the hand produced larger BOLD responses in the posterior thalamus of subjects undergoing a migraine attack with extracephalic allodynia than the corresponding responses registered when the same patients were free of migraine and allodynia. Interpretation We propose that the spreading of multimodal allodynia and hyperalgesia beyond the locus of migraine headache is mediated by sensitized thalamic neurons that process nociceptive information from the cranial meninges together with sensory information from the skin of the scalp, face, body, and limbs. ANN NEUROL 2010 [source]

Triptan-induced latent sensitization: A possible basis for medication overuse headache

ANNALS OF NEUROLOGY, Issue 3 2010
Milena De Felice PhD
Objective Identification of the neural mechanisms underlying medication overuse headache resulting from triptans. Methods Triptans were administered systemically to rats by repeated intermittent injections or by continuous infusion over 6 days. Periorbital and hind paw sensory thresholds were measured to detect cutaneous allodynia. Immunofluorescent histochemistry was employed to detect changes in peptidic neurotransmitter expression in identified dural afferents. Enzyme-linked immunoabsorbent assay was used to measure calcitonin gene-related peptide (CGRP) levels in blood. Results Sustained or repeated administration of triptans to rats elicited time-dependent and reversible cutaneous tactile allodynia that was maintained throughout and transiently after drug delivery. Triptan administration increased labeling for CGRP in identified trigeminal dural afferents that persisted long after discontinuation of triptan exposure. Two weeks after triptan exposure, when sensory thresholds returned to baseline levels, rats showed enhanced cutaneous allodynia and increased CGRP in the blood following challenge with a nitric oxide donor. Triptan treatment thus induces a state of latent sensitization characterized by persistent pronociceptive neural adaptations in dural afferents and enhanced responses to an established trigger of migraine headache in humans. Interpretation Triptans represent the treatment of choice for moderate and severe migraine headaches. However, triptan overuse can lead to an increased frequency of migraine headache. Overuse of these medications could induce neural adaptations that result in a state of latent sensitization, which might increase sensitivity to migraine triggers. The latent sensitization could provide a mechanistic basis for the transformation of migraine to medication overuse headache. ANN NEUROL 2010;67:325,337 [source]

Does the Addition of Dexamethasone to Standard Therapy for Acute Migraine Headache Decrease the Incidence of Recurrent Headache for Patients Treated in the Emergency Department?

Donitriptan, but not sumatriptan, inhibits capsaicin-induced canine external carotid vasodilatation via 5-HT1B rather than 5-HT1D receptors

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006
E Muñoz-Islas
Background and purpose: It has been suggested that during a migraine attack capsaicin-sensitive trigeminal sensory nerves release calcitonin gene-related peptide (CGRP), resulting in cranial vasodilatation and central nociception; hence, trigeminal inhibition may prevent this vasodilatation and abort migraine headache. This study investigated the effects of the agonists sumatriptan (5-HT1B/1D water-soluble), donitriptan (5-HT1B/1D lipid-soluble), PNU-142633 (5-HT1D water-soluble) and PNU-109291 (5-HT1D lipid-soluble) on vasodilator responses to capsaicin, , -CGRP and acetylcholine in dog external carotid artery. Experimental approach: 59 vagosympathectomized dogs were anaesthetized with sodium pentobarbitone. Blood pressure and heart rate were recorded with a pressure transducer, connected to a cannula inserted into a femoral artery. A precalibrated flow probe was placed around the common carotid artery, with ligation of the internal carotid and occipital branches, and connected to an ultrasonic flowmeter. The thyroid artery was cannulated for infusion of agonists. Key results: Intracarotid infusions of capsaicin, , -CGRP and acetylcholine dose-dependently increased blood flow through the carotid artery. These responses remained unaffected after intravenous (i.v.) infusions of sumatriptan, PNU-142633, PNU-109291 or physiological saline; in contrast, donitriptan significantly attenuated the vasodilator responses to capsaicin, but not those to , -CGRP or acetylcholine. Only sumatriptan and donitriptan dose-dependently decreased the carotid blood flow. Interestingly, i.v. administration of the antagonist, SB224289 (5-HT1B), but not of BRL15572 (5-HT1D), abolished the inhibition by donitriptan. Conclusions and implications: Our results suggest that the inhibition produced by donitriptan of capsaicin-induced external carotid vasodilatation is mainly mediated by 5-HT1B, rather than 5-HT1D, receptors, probably by a central mechanism. British Journal of Pharmacology (2006) 149, 82,91. doi:10.1038/sj.bjp.0706839 [source]