bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development and Validation of the Headache Needs Assessment (HANA) Survey
Authors: Cramer Joyce A. , Silberstein Stephen D. , Winner Paul 
Published: March 2003

Objective.—To develop and validate a brief survey of migraine‐related quality‐of‐life issues. The Headache Needs Assessment (HANA) questionnaire was designed to assess two dimensions of the chronic impact of migraine (frequency and bothersomeness).Methods.—Seven issues related to living with migraine were posed as ratings of frequency and bothersomeness. Validation studies were performed in a Web‐based survey, a clinical trial responsiveness population, and a retest reliability population. Headache characteristics (eg, frequency, severity, and treatment), demographic information, and the Headache Disability Inventory were used for external validation.Results.—The HANA was completed in full by 994 adults in the Web survey, with a mean total score of 77.98 ± 40.49 (range, 7 to 175). There were no floor or ceiling effects. The HANA met the standards for validity with internal consistency reliability (Cronbach α = .92, eigenvalue for the single factor = 4.8, and test‐retest reliability = 0.77). External validity showed a high correlation between HANA and Headache Disability Inventory total scores (0.73, P<.0001), and high correlations with disease and treatment characteristics.Conclusions.—These data demonstrate the psychometric properties of the HANA. The brief questionnaire may be a useful screening tool to evaluate the impact of migraine on individuals. The two‐dimensional approach to patient‐reported quality of life allows individuals to weight the impact of both frequency and bothersomeness of chronic migraines on multiple aspects of daily life.
Comparison of Triptan Tablet Consumption per Attack: A Prospective Study of Migraineurs in Spain
Authors: Pascual Julio , Fité Benet , López‐Gil Arturo 
Published: March 2003

Objectives.—To compare patient self‐reported tablet consumption of rizatriptan 10 mg per attack (24 hours) with that of sumatriptan 50 mg, zolmitriptan 2.5 mg, and naratriptan 2.5 mg on an unselected, prescription‐based, Spanish migraine population.Methods.—One hundred twenty community pharmacies recruited patients with migraine, who used their pharmacies, to fill a triptan prescription. In diaries, patients recorded baseline pain intensity and the number of triptan tablets and additional medication taken per attack. Patients treated a maximum of three attacks. Analysis of variance or the Student t test and chi‐square or Fisher exact tests were used for univariate comparisons. Hochberg corrections were used for multiple‐group comparisons. A generalized estimating equation method was used to correct for within‐subject correlation. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were calculated.Results.—Two hundred thirty‐one patients (84% women) treated 589 evaluable migraine attacks (sumatriptan, n = 135; naratriptan, n = 90; zolmitriptan, n = 149; rizatriptan, n = 149). Triptan tablet consumption per attack (mean ± SD) for rizatriptan (1.24 ± 0.56) was significantly lower than that of sumatriptan (1.75 ± 1.2; P  <  .05), zolmitriptan (1.61 ± 0.86; P  <  .05), or naratriptan (1.46 ± 0.62; P = .05). The average number of triptan tablets taken and additional medication use increased according to baseline pain severity. More attacks were treated with one tablet of rizatriptan (81.2%) than with one tablet of sumatriptan (51.9%), zolmitriptan (55.7%), or naratriptan (60%). The probability of using more than one triptan tablet per attack (24 hours) was more than three times greater for sumatriptan (adjusted OR = 3.71; CI, 2.05 to 6.7; P = .001) and zolmitriptan (adjusted OR = 3.32; CI, 1.82 to 6.17; P = .001), and more than two times greater for naratriptan (adjusted OR = 2.66; CI, 1.36 to 5.21; P = .004) than for rizatriptan.Conclusions.—Rizatriptan was associated with significantly lower triptan tablet use and additional medication use per attack than the other triptans. Additional randomized studies are needed to confirm the conclusions of this study.
Migraine Is Associated With Livedo Reticularis: A Prospective Study
Authors: Tietjen Gretchen E. , Gottwald Lorie , Al‐Qasmi Mohamed M. , Gunda Padma , Khuder Sadik A. 
Published: March 2003

Objective.—To investigate the relationship of livedo reticularis, an ischemic dermatopathy, and migraine, an ischemic stroke risk factor.Background.—Livedo reticularis refers to the reddish‐blue reticular mottling of the skin resulting from narrowing of small and medium arteries at the dermis‐subcutis border. A subset of patients with livedo reticularis develop stroke in the absence of other vascular risk factors, which has been termed Sneddon syndrome. We undertook this prospective study in a non‐neurology clinic to delineate further the relationship of livedo reticularis and migraine.Methods.—Patients in a general dermatology clinic were interviewed for vascular risk factors and history of migraine in accordance with the International Headache Society (IHS) criteria. A dermatologist, not familiar with the interview, recorded the primary dermatological diagnosis and the presence or absence of livedo reticularis on examination.Results.—Two hundred eighty‐one consecutive patients (184 women and 97 men; average age, 52 years) were interviewed and examined. Seventy‐five (27%) had migraine (IHS codes 1.1, 1.2) and an additional 18 (6%) had atypical migraine (IHS 1.7). Livedo reticularis was noted in 46 patients (16%), with the frequency higher in women than men (42 [23%] of 184 versus 4 [4%] of 97; P < .0001). The frequency of livedo reticularis in patients with migraine was higher than in those without migraine (24 [26%] of 93 versus 22 [12%] of 188; P = .002), and higher in female than male migraineurs (23 [32%] of 72 versus 1 [5%] of 21; P = .012). In logistic regression analysis of the women, migraine was associated with livedo reticularis (odds ratio [OR], 2.3; confidence interval [CI], 1.08 to 4.71), as well as with stroke (OR, 4.0; CI, 0.87 to 18.21), coronary artery disease (OR, 3.5; CI, 1.16 to 10.33), and deep venous thrombosis (OR, 3.2; CI, 0.98 to 10.32).Conclusions.—In women, migraine is associated with stroke, coronary artery disease, deep venous thrombosis, as well as livedo reticularis, a dermatopathy which has been pathologically linked to cerebral vasculopathy. Whether migraineurs with livedo reticularis compose a subset at higher risk of thrombosis, including stroke, deserves further investigation.
Livedo Reticularis and Migraine: A Marker for Stroke Risk?
Authors: Tietjen Gretchen E. , Al‐Qasmi Mohamed M. , Shukairy Mohammad S. 
Published: March 2003

Background and Purpose.—Livedo reticularis is a dermatopathy characterized by an irregular, violaceous, netlike pattern which spares the face. Associated with a variety of conditions, it occurs consequent to pathological or physiological narrowing of small and medium arteries at the dermis‐subcutis border. Sneddon syndrome refers to the idiopathic coupling of livedo reticularis and stroke in the absence of traditional vascular risk factors. Over 50% of persons with Sneddon syndrome describe a history of headache. We undertook this study to determine the frequency of livedo reticularis in our headache clinic.Methods.—We performed a retrospective chart review of consecutive patients attending a headache clinic over a period of 6 months. The patients had all been seen by one physician (G.E.T.) who noted the presence or absence of livedo reticularis. The charts were reviewed for age, sex, and vascular risk factors, including current use of oral contraceptives, and history of smoking, coronary artery disease, hypertension, diabetes mellitus, stroke, or arthritis.Results.—Charts from 133 patients with headache were reviewed (24 men [18%], 109 women [82%]; mean age, 42  ±  13 years). Livedo reticularis was observed in 29 patients (22%) and in a similar proportion in men (25%) and women (21%). When we stratified the migraine population by presence or absence of livedo, we found no significant difference in age (44.5 versus 41.7 years, P  =   .16). There was a higher frequency of stroke diagnosis in the cohort with livedo reticularis (28%[8 of 29] versus 7%[7 of 104], P  =   .005), but we found no significant differences in frequency of hypertension, oral contraceptive use, diabetes mellitus, coronary artery disease, arthritis, or cigarette smoking.Conclusions.—In our headache clinic, livedo reticularis is present in more than one fifth of patients. A history of stroke is more frequent in this subset of migraineurs, raising the possibility that livedo reticularis can be used as a clinical marker to identify those migraineurs with an increased risk of stroke.
Decreased Sensitivity of 5‐HT1D Receptors in Chronic Tension‐Type Headache
Authors: Rainero I. , Valfrè W. , Savi L. , Ferrero M. , Del Rizzo P. , Limone P. , Isaia G.C. , Gianotti L. , Pollo A. , Verde R. , Benedetti F. , Pinessi L. 
Published: March 2003

Objective.—To assess the sensitivity of 5‐HT1D receptors in chronic tension‐type headache using sumatriptan as a pharmacological probe.Background.—Previous studies have suggested involvement of serotonergic systems in chronic tension‐type headache (CTTH), but relevant experimental data are limited. Sumatriptan, a 5‐HT1B/1D receptor agonist, stimulates the release of growth hormone (GH) and inhibits the release of ACTH, cortisol, and prolactin. These effects may be used to explore the function of serotonergic systems in vivo.Methods.—We measured GH, ACTH, cortisol and prolactin (PRL) plasma concentrations in 15 patients with chronic tension‐type headache and in 18 healthy controls after subcutaneous administration of sumatriptan (6 mg) or placebo.Results.—Placebo administration had no effect on hormone concentrations. GH and PRL secretion after sumatriptan administration was significantly (P<0.01 and <0.05) altered in CTTH patients in comparison with controls.Conclusion.—Our results suggest that cerebral serotonergic functions mediated by 5‐HT1D receptors are altered in CTTH.
Melatonin as Adjunctive Therapy in the Prophylaxis of Cluster Headache: A Pilot Study
Authors: Pringsheim Tamara , Magnoux Eric , Dobson Colin F. , Hamel Edith , Aubé Michel 
Published: March 2003

Background.—The periodicity of cluster headache suggests involvement of the suprachiasmatic nucleus of the hypothalamus, the biological clock. The secretion of melatonin, a hormone produced by the pineal gland and regulated by the suprachiasmatic nucleus, is altered in patients with cluster headache. Melatonin shifts circadian rhythms. A previous study of melatonin for primary prophylaxis of cluster headache demonstrated a 50% response rate.Objective.—To evaluate the use of melatonin as adjunctive therapy in patients with cluster headache who have incomplete relief of their headaches on conventional therapy.Methods.—Nine patients participated in the study, six with chronic cluster headache and three with episodic cluster headache. Patients with chronic cluster headache completed a baseline diary for 1 month, followed by 1 month of melatonin treatment, then 1 month of placebo. Patients with episodic cluster headache received placebo for 1 month, then melatonin for 1 month. Patients continued their usual prophylactic and abortive treatments during the study. Headache frequency, intensity, and use of analgesics were recorded. The primary endpoint of the study was the mean number of headaches per day, with mean daily analgesic consumption and percentage of mild, moderate, and severe headaches as secondary endpoints.Results.—There were no significant differences between means on analysis of variance and t testing for the melatonin, placebo, and baseline months for all primary and secondary endpoints. There were no side effects reported.Conclusions.—Patients with chronic cluster headache or patients with episodic cluster headache whose headaches are uncontrolled on conventional therapy do not appear to gain therapeutically from the addition of melatonin to their usual treatment regimens. It is perhaps the phase‐shifting properties of melatonin that mediate its effect in patients with episodic cluster headache, and it may be necessary to treat from the beginning of the cluster bout to reset the circadian pacemaker, thus producing a more positive outcome.
A Polymorphism in the Serotonin Transporter Gene Regulatory Region and Frequency of Migraine Attacks
Authors: Kotani Kazuhiko , Shimomura Tokio , Shimomura Fumiyo , Ikawa Shiro , Nanba Eiji 
Published: March 2003

Background.—The serotonergic system has been thought to play an important part in the pathophysiology of migraine. Objective.—To study an association between the polymorphism of serotonin (5‐hydroxytryptamine [5‐HT]) transporter gene‐linked polymorphic region (5‐HTTLPR) and migraine. Method.—We compared 151 patients with migraine with 190 healthy unrelated control subjects. The 5‐HTTLPR polymorphism was detected using polymerase chain reaction. Migraine patients were interviewed regarding attack frequency in the last 6 months. Results.—We denoted the products of the 484‐base pair (bp) fragments as the short (s) and those of 528 bp as the long (l) allele according to the previously reported manner. Migraine patients with s/s genotype were compared with those with l/s and l/l genotype. We did not find significant differences in the genotype and allele frequencies of 5‐HTTLPR between patients with migraine and control subjects. Among patients with migraine, those with s/s type had significantly more frequent attacks than those with the l/s or l/l type. Conclusions.—This polymorphism does not appear to be involved in a genetic predisposition to the disease but may affect the frequency of attacks in patients with migraine. These findings may contribute to our understanding of factors that influence the clinical severity of migraine.
Hormone Supplementation Differently Affects Migraine in Postmenopausal Women
Authors: Facchinetti F. , Nappi R. E. , Tirelli A. , Polatti F. , Nappi G. 
Published: March 2003

Objective.—To evaluate the effects of three schemes of oral hormone replacement therapy (HRT) on migraine course in postmenopausal women. Methods.—Thirty‐eight patients presenting for clinical evaluation of menopausal status and suffering from migraine were enrolled. The observational period lasted 7 months, during which women filled in a daily diary with the clinical features of headache attacks and analgesic use. We evaluated climacteric symptoms, anxiety and depression. After a 1‐month run‐in period, women were assigned to one of three regimens of HRT: estradiol hemihydrate 1 mg/day plus norethisterone 0.5 mg/day for 28 days, in a continuous combined scheme; oral conjugated estrogens 0.625 mg/day for 28 days plus medroxyprogesterone acetate 10 mg/day in the last 14 days, in a sequential continuous scheme; and estradiol valerate 2 mg/day for 21 days plus cyproterone acetate 1 mg/day from day 12 to 21 in a sequential cyclical scheme. Follow‐up evaluations were performed at 3 and 6 months. Results.—During the run‐in period, the three subgroups of patients were similar as far as the features of migraine are concerned. Overall, a progressive increase in attack frequency (from 2.2  ±  1.0 to 3.8  ±  1.3, P<.001), days with headache (from 3.4  ±  1.3 to 4.9  ±  1.9, P<.001), and analgesic consumption (from 3.4  ±  1.3 to 5.6  ±  2.2, P<.001) was observed after 6 months. Duration of attacks decreased (from 18.1  ±  7.4 to 13.6  ±  4.2 hours, P  =  .005), whereas severity worsened (from 1.9  ±  0.2 to 2.1  ±  0.2, P<.001). The increase in number of days with headache and number of analgesics used was smaller in the group receiving the continuous combined regimen than in the other two groups. Conclusion.—Although HRT typically will lead to some worsening of headache syndrome, estradiol hemihydrate plus norethisterone given in a combined continuous scheme was the regimen best tolerated by our patients.
Migraine and Psychiatric Comorbidity: From Theory and Hypotheses to Clinical Application
Authors: Sheftell Fred D. , Atlas Susan J. 
Published: March 2003

Objective.—To review psychiatric issues that accompany migraine and means of addressing these issues. Background.—Psychiatric factors and migraine may interact in three general ways, etiologically, psychophysiologically or biobehaviorally, and comorbidly (the two disorders coexist), which is the present focus. There are several possible mechanisms of comorbidity. The relation between two disorders may be a result of chance. One disorder can cause another disorder: Diabetes can cause diabetic neuropathy. There might be shared environmental risks: Head trauma can cause both posttraumatic epilepsy and posttraumatic headache. And there may be environmental or genetic risk factors that produce a brain state giving rise to both conditions, that is, there may be some common biology underlying both conditions. This last mechanism seems to be the most likely one underlying comorbidity of migraine and psychiatric disorders. We introduce a possible role for classical paradigms of learned helplessness in regard to psychiatric comorbid depressive and anxiety disorders and migraine. Results.—There appears to be an association between migraine and affective disorders, particularly depression and anxiety. There are a number of formal tools for recognizing depression, but clinical evaluation should not be overlooked. Once diagnosed, depression and anxiety should be treated, both to improve the success of migraine treatment and to improve the patient's quality of life. Patients with recurring headaches are much more likely to overuse and misuse, rather than abuse, pain medications. It is important to be alert for signs that the patient may be misusing medication. Behavioral approaches can surround and support pharmacological therapy. Conclusions.—Migraine is often comorbid with psychiatric disorders, particularly depression and anxiety. The relationship is likely based on shared mechanisms and successful treatment is possible.
Headache and Other Types of Chronic Pain
Authors: Marcus Dawn A. 
Published: March 2003

Objective.—To compare pain severity, disability, psychological distress, and quality of life between patients with headache and nonheadache treatment‐seeking chronic pain patients.Methods.—Six hundred forty‐three patients seeking treatment at a university pain clinic were divided into 3 categories based on primary pain complaint and the presence of focal or diffuse pain complaints: headache, nonheadache focal (pain involving <50% of the body), and nonheadache diffuse (pain involving ≥50% of the body). Patients completed questionnaires to identify pain severity, disability, depression, anxiety, and quality of life.Results.—Patients with headache differed from nonheadache patients for all evaluated parameters. Average pain severity on a 0 to 10 point severity scale was 5.55 for headache, 6.93 for nonheadache focal, and 8.05 for nonheadache diffuse. Pain occurred an additional 1.51 to 1.71 days per week for patients without headache. Compared to patients with headache, patients without headache reported greater frequency of reduced daily activities and complete disability related to pain. In addition, patients without headache and with diffuse pain reported more depression (78.2% vs. 45.8%) and anxiety (70.0% vs. 39.1%) than patients with headache. Quality of life measures were significantly reduced in patients with either nonheadache focal or diffuse conditions compared to patients with headache.Conclusions.—Even when considering patients with focal rather than diffuse chronic pain complaints, patients with headache are dissimilar from other patients with chronic pain. Pain severity, frequency, disability, psychological distress, and quality of life are significantly more prominent or impaired in patients with chronic pain without headache compared to patients with headache.
Transcranial Doppler in Migraine Attacks Before and After Treatment With Oral Zolmitriptan or Sumatriptan
Authors: Thomaides Thomas , Karagounakis Demetrios , Spantideas Anastasios , Katelanis Stavros 
Published: March 2003

Background.—Intracranial blood flow velocity (BFV) changes in migraine have been studied fairly extensively. Although a number of investigations have been performed in migraineurs with nitroglycerin‐induced attacks, there has been no reported transcranial study involving such attack treated with zolmitriptan or sumatriptan.Methods.—With ultrasound, we studied the BFV and pulsatility index (PI) changes in the middle cerebral artery in 45 symptom free, otherwise healthy, unmedicated patients with migraine without aura, and in 15 age‐ and sex‐matched controls before nitroglycerin, at the time of maximum head pain induced by nitroglycerin and every 30 minutes for 2 hours after zolmitriptan (15 subjects) or sumatriptan (15 subjects) administration. Headache was rated on a 4‐point scale.Results.—During headache attacks, BFV decreased significantly (36.7±3.3, 38.4±3.4, and 37.4±4 cm/sec, respectively, in the zolmitriptan, sumatriptan, and nontreated migraine groups, but not in the controls who were migraine free (P  <  .01). These abnormalities disappeared 1 hour after zolmitriptan or sumatriptan administration (49.7±3.7 and 48.9±3.9cm/sec, respectively). There were no significant changes in PI.Conclusion.—Our data indicate that nitroglycerin‐induced headache in individuals with migraine without aura is associated with BFV changes that are reversed by administration of an oral triptan.
Ibotenate Injections into the Pre‐ and Parasubiculum Provide Partial Protection against Kainate‐Induced Epileptic Damage in Layer III of Rat Entorhinal Cortex
Authors: Eid Tore , Du Fu , Schwarcz Robert 
Published: March 2003

Summary:  Purpose: A loss of neurons in layer III of the entorhinal cortex (EC) is often observed in patients with temporal lobe epilepsy and in animal models of the disorder. We hypothesized that the susceptibility of layer III of the EC to prolonged seizure activity might be mediated by excitatory afferents originating in the presubiculum.Methods: Experiments were designed to ablate the presubiculum unilaterally by focal ibotenate injections and to evaluate the effect of this deafferentation on the vulnerability of EC layer III neurons to the chemoconvulsant kainate (injected systemically 5 days later).Results: After treatment with kainate, 11 of the 15 rats preinjected with ibotenate showed clear‐cut, partial neuroprotection in layer III of the EC ipsilateral to the ibotenate lesion. Serial reconstruction of the ibotenate‐induced primary lesion revealed that entorhinal neurons were protected only in animals that had lesions in the pre‐ and parasubiculum, especially in the deep layers (IV–VI).Conclusions: The deep layers of the pre‐ and parasubiculum appear to control the seizure‐induced damage of EC layer III. This phenomenon may be of relevance for epileptogenesis and for the pathogenesis of temporal lobe epilepsy.