Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bupropion was initially developed and licensed for the treatment of major depressive disorder in the United States in 1989. It was licensed as a pharmacotherapy for smoking cessation in the United States in 1997 and in the United Kingdom in 2000, and for the prevention of seasonal major depressive episodes in patients with seasonal affective disorder in the United States in 2006. Its main mechanism of action is believed to be via dopamine and noradrenalin reuptake inhibition. In addition to proven clinical efficacy for the treatment of major depression, the prevention of depressive episodes in patients with seasonal affective disorder, and as an aid to smoking cessation treatment, bupropion has demonstrated efficacy for attenuation of symptoms of attention deficit hyperactivity disorder, and more recently it has shown anti-inflammatory action against proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha), which may be implicated in a number of inflammatory diseases such as Crohn's disease. The twice-daily sustained-release formulation has been extensively evaluated for smoking cessation and has shown continuous smoking abstinence rates at one year of the order of 20% across many clinical groups including healthy smokers, and smokers with cardiovascular disease, chronic obstructive airways disease, depression and schizophrenia. Bupropion is well tolerated with side effects including insomnia, headache, dry mouth, dizziness and nausea. Bupropion is a cytochrome p450 2D6 inhibitor and care must be taken when coprescribing with drugs cleared by this enzyme and when coprescribing with drugs that lower seizure threshold. Despite the clinical effectiveness and cost-effectiveness of bupropion as an aid to smoking cessation, its uptake for this indication remains low when compared with nicotine replacement therapy.
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PMID:Bupropion. 1713 26

The case of a 72-year-old demented woman having episodes of strokes without any risk factors for cardiovascular disease is reported. Her elder brother and sister have also had stroke episodes since their middle age. She experienced hallucinations, delusions, and recurrent headaches since the age of 55. She has gradually developed gait disturbance and cognitive impairment. Brain MRI revealed extensive leukoaraiosis and multiple lacunar infarcts in the deep white matter and brainstem. Repeated MRI incidentally disclosed fresh hemorrhage in the dorsal subcortical temporal lobe, which appeared to be asymptomatic. Anti-platelet agents were not used during disease progression. We detected G975C mutation of the Notch3 gene and diagnosed our patient's disease as cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). This report suggests that arteriopathy of CADASIL could cause a hemorrhagic process, indicating that, in such a case, routine administration of anti-platelet agent to prevent recurrent ischemic stroke is not recommended.
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PMID:[Case of CADASIL showing spontaneous subcortical hemorrhage with a novel mutation of Notch3 gene]. 1726 Aug 7

Tobacco smoking remains a significant health problem in the United States. It has been associated with staggering morbidity and mortality, specifically due to malignancies and cardiovascular disease. Smoking cessation can be difficult and frequently requires pharmacologic interventions in addition to nonpharmacologic measures. Previously available agents are nicotine replacement products and bupropion, which increased quit rates by about 2-fold compared with placebo. Varenicline is the first drug in a new class known as the selective alpha4beta2 nicotinic receptor partial agonists. In several randomized, double-blind, 52-week clinical trials involving healthy chronic smokers, varenicline demonstrated superiority to placebo and bupropion in terms of efficacy measures. Additionally, it improved tobacco withdrawal symptoms and reinforcing effects of smoking in relapsed patients. Patients should start therapy in combination with tobacco cessation counseling 1 week before quit date and continue the regimen for 12 weeks. The dose of varenicline should be titrated to minimize nausea. The recommended dosage is 0.5 mg once daily (QD) on days 1-3; titrate to 0.5 mg twice daily (BID) on days 4-7; and 1 mg BID starting on day 8. An additional 12-week maintenance therapy may be considered for those who achieve abstinence. The most common side effects are nausea (30%), insomnia (18%), headache (15%), abnormal dreams (13%), constipation (8%), and abdominal pain (7%). Overall, varenicline is a breakthrough in the management of tobacco addiction and has demonstrated good efficacy in motivated quitters. It also provides an option for smokers who cannot tolerate other pharmacologic interventions.
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PMID:Varenicline: a selective alpha4beta2 nicotinic acetylcholine receptor partial agonist approved for smoking cessation. 1743 82

An association between migraine and ischaemic vascular events, particularly ischaemic stroke, has been debated for many years. The pathophysiology of migraine has been explored in detail, and it is known that a dysfunction of brain cells and arteries is a major component of this disorder. The involvement of cerebral arteries during the migraine attack as well as the high prevalence of migraine among young individuals with ischaemic stroke has led to the hypothesis that migraine may be a risk factor for ischaemic stroke. Furthermore, there is evidence that the vascular nature of migraine is not limited to meningeal blood vessels and that migraine and overall cardiovascular disease may share aetiological pathways. The aim of this review is to summarize the epidemiological evidence that links migraine with ischaemic stroke and ischaemic heart disease and to discuss potential biological mechanisms.
Cephalalgia 2007 Aug
PMID:Migraine and ischaemic vascular events. 1766 73

Migraine has been associated with an unfavourable cardiovascular risk profile and with increased risk of cardiovascular disease. In a cross-sectional analysis of 27,626 women aged >or=45 years, we evaluated the association of migraine and migraine aura status with elevated levels of total cholesterol, low- and high-density lipoprotein cholesterol (HDL-C), non-HDL-C, apolipoprotein (Apo) A-1 and B(100), lipoprotein (a), C-reactive protein (CRP), fibrinogen, intercellular adhesion molecule-1, homocysteine and creatinine. A total of 5087 (18.4%) women reported any history of migraine. Compared with women with no migraine history, women who reported any history of migraine had modestly increased adjusted odds ratios (95% confidence interval) of 1.09 (1.01, 1.18) for elevated total cholesterol, 1.14 (1.05, 1.23) for non-HDL-C, 1.09 (1.01, 1.18) for Apo B(100) and 1.13 (1.05, 1.22) for CRP. The increase did not meaningfully differ according to migraine aura status and migraine frequency. In this large cohort of women, only a modest association was found between migraine and adverse levels of certain cardiovascular biomarkers.
Cephalalgia 2008 Jan
PMID:Migraine and biomarkers of cardiovascular disease in women. 1798 70

After several decades of senescence, the twin fields of hyperuricemia and gout have again regained attention in both the scientific and clinical spheres, and this review highlights several recent advancements. Specifically, we review newly discovered mechanisms of uric acid-induced inflammation, uric acid's putative role as a "danger signal" in innate immunity, the possible link between hyperuricemia and cardiovascular disease, and evolutionary evidence suggesting that hyperuricemia conferred a survival advantage in primates (when the gene for uricase was lost) several million years ago. Finally, we provide an overview of the current approach to gout, as well as what treatments are on the horizon.
Curr Pain Headache Rep 2007 Dec
PMID:Update on gout: pathophysiology and potential treatments. 1817 79

Migraine is a chronic recurrent disorder with episodic manifestations that is progressive in some individuals. Migraine progresses clinically, physiologically, and anatomically. Progression may be a consequence of the mechanisms that generate the migraine attacks (eg, cortical spreading depression) or it may be a function of the activations generated by the attacks (eg, lesions in the periaqueductal gray area), a hypothesis supported by the increase in lesions with attack frequency. Progression may also be partially explained by common genetic or environmental risk factors. Finally, migraine with aura is associated with an elevated Framingham score and with risk factors for cardiovascular disease. Research on this issue is in its infancy and cautions are necessary before extrapolating this information into clinical practice.
Headache 2008 Jan
PMID:Concepts and mechanisms of migraine chronification. 1818 80

This study investigates the importance of alcohol as a migraine trigger factor, the prevalence of alcohol consumers and the mechanism of headache provocation. A MEDLINE search from 1988 to October 2007 was performed for "headache and alcohol", "headache and wine", "migraine and alcohol" and "migraine and wine". In retrospective studies, about one-third of the migraine patients reported alcohol as a migraine trigger, at least occasionally, but only 10% of the migraine patients reported alcohol as a migraine trigger frequently. Regional differences were reported, perhaps depending in part on alcohol habits. No differences were found between migraine and tension headache and different genders. However, prospective studies limit considerably the importance of alcohol as a trigger. Recent studies show that migraine patients consume less alcohol than controls. Red wine was reported to be the principal trigger of migraine, but other studies show that white wine or other drinks are more involved. Then, the discussion based on the different composition of the various alcoholic beverages, in order to discover the content of alcoholic drinks responsible for migraine attack, reflects this uncertainty. Biogenic amines, sulphites, flavonoid phenols, 5-hydroxytryptamine mechanisms and vasodilating effects are discussed. The fact that few headache patients cannot tolerate some alcoholic drinks does not justify the consideration that alcohol is a major trigger and the suggestion of abstinence. In fact, low doses of alcohol can have a beneficial effect on patients such as migraineurs, who were reported to have an increased risk of cardiovascular disease.
J Headache Pain 2008 Feb
PMID:Alcohol and migraine: trigger factor, consumption, mechanisms. A review. 1823 12

The prevalence of migraine headaches (MH) is 12% in the general population and increases to 40% in patients with patent foramen ovale. This study evaluated the prevalence of MH in patients with congenital heart disease (CHD). Of 466 patients contacted from the UCLA Adult Congenital Heart Disease Center, 395 (85%) completed a questionnaire to determine the prevalence of MH. Patients were stratified by diagnosis of right-to-left, left-to-right, or no shunt. A group of 252 sex-matched patients with acquired cardiovascular disease served as controls. The prevalence of MH was 45% in adults with CHD compared to 11% in the controls (p<0.001). Of the 179 patients with MH, 143 (80%) had migraines with aura and 36 (20%) had migraines without aura versus 36% and 64% observed in the controls (p<0.001). The frequency of MH was 52% in the right-to-left shunt group, 44% in the left-to-right, and 38% in the no shunt group (p=NS). In patients with a right-to-left shunt who underwent surgical repair, 47% had complete resolution of MH, whereas 76% experienced >50% reduction in headache days per month. In conclusion, the prevalence of MH in all groups of adults with CHD is 3 to 4 times more than a sex-matched control population, with increasing prevalence of MH in patients with no shunt, left-to-right, and right-to-left shunt. The higher than expected frequency of MH in patients with CHD without an intracardiac shunt, suggests additional mechanisms to explain the significant association with MH.
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PMID:Prevalence of migraine headaches in patients with congenital heart disease. 1823 8

An aim of the study was to compare by the analysis of pedigrees the frequency of vascular pathology in first-degree relatives (FDR) of patients with intracranial aneurysms (IA) and controls. Pedigrees were selected by interviewing 194 patients with IA (94 men and 100 women) and 193 age- and sex-matched control patients. Only FDR with complete information about their health status were included: 1011 FDR of patients with IA and 812 FDR of controls. The results of the study revealed that the frequency of strokes was 2.5 times higher in FDR of patients with IA than in those of controls: 6.5% and 2.6%, respectively (RR = 2.52, 95% CI = 1.56-4.09). Hemorrhages occurred 3.7 times more often in FDR of patients with IA than in FDR of controls: 3.4% versus 0.9% (RR = 3.90, 95% CI = 1.74-8.75). Only 0.9% of FDR of patients with IA had the rupture of intracranial aneurysm compared with nobody in FDR of controls. The frequency of headaches was 2.8 times greater in FDR of patients with IA than in those of controls: 19.6% versus 7.1% (RR = 2.74, 95% CI = 2.08-3.62). FDR of patients with IA suffered from arterial hypertension 2 times more often than FDR of controls: 24.9% and 11.6%, respectively (RR = 2.15, 95% CI = 1.73-2.68). Coronary heart disease was 2.7 times more frequent in FDR of patients with IA than in controls: 8.9% and 3.3%, respectively (RR = 2.68, 95% CI = 1.76-4.07). Sudden death occurred in FDR of patients with IA 5.8 times more often than FDR of controls: 11.1% and 1.9%, respectively (RR = 5.68, 95% CI = 1.37-23.39). Thus, vascular pathology occurs relatively often in FDR of patients with IA implying that vascular defects which cause the development of IA may be, at least in part, genetically determined. Prevention of stroke and cardiovascular disease is necessary for FDR of patients with IA.
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PMID:[Vascular pathology in first-degree relatives of patients with intracranial aneurysms]. 1892 79


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