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

Animal models for migraine have provided substantial advances on the mechanisms and mediators underlying migraine attacks. The neurogenic inflammation model has helped understanding the perivascular mechanisms underlying the pathophysiology of migraine attacks, the receptors involved and the effect of specific antimigraine drugs. The model based on probing the neuronal effects of nitroglycerin--an organic nitrate known to induce spontaneous-like migraine attacks in predisposed subjects--in the rat has provided interesting insights into the neuroanatomic circuits and neuropharmacological mechanisms involved in the initiation and repetition of migraine attacks [corrected].
Cephalalgia 2003
PMID:Peripheral and central activation of trigeminal pain pathways in migraine: data from experimental animal models. 1269 54

Methaemoglobinemia is a disorder in which the haemoglobin molecule is functionally altered and prevented from carrying oxygen. A variety of aetiologies including genetic, dietary, idiopathic and toxicological sources may cause methaemoglobinemia. Symptoms vary from mild headache to coma or death, and may not correlate with measured methaemoglobin concentrations. Patients with methaemoglobinemia appear deeply cyanotic, but are unresponsive to standard oxygen therapy. It is essential for the clinician to recognize the problem rapidly in patients without hypoxia by analysing their arterial blood gas. Methaemoglobin interferes with the accuracy of pulse oximetry. The antidote is methylene blue. We report a very unusual and dramatic case of methaemoglobinemia. A 23-year-old girl who arrived in the emergency department in a state of confusion with intense cyanosis. The night before she had drunk water with ice defiled by ammonium nitrate, poured from a broken pack of instant ice. The absence of improvement after the administration of oxygen and the 'chocolate brown' colour of the arterial blood gave us the most important clue in suspecting the diagnosis of methaemoglobinemia.
 ...
PMID:A severe methaemoglobinemia induced by nitrates: a case report. 1467 14

Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1-6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. Exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischaemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions.
Cephalalgia 2004 Feb
PMID:Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters. 1472 4

During the administration of recombinant human TSH (rhTSH) to monitor differentiated thyroid carcinoma, mild side effects, such as nausea and headaches, often occur. The origin of these is not clear. Since changes in TSH and thyroid hormones can modulate some endothelial-derived factors, we aimed at testing whether rhTSH administration induces changes in nitric oxide. We studied 25 patients (56.6+/-12.6 yr) who had undergone thyroidectomy followed by ablative radioiodine for papillary thyroid cancer and who were under follow-up. While L-thyroxine therapy continued, thyroglobulin (Tg), TSH, free-T3, free-T4 and nitrite-plus-nitrate (NOx) concentrations were evaluated before and after rhTSH administration (0.9 mg i.m. on 2 consecutive days). Mean TSH showed a huge increase from baseline (0.1+/-0.0 mIU/l) to day 3 (216.3+/-17.5 mIU/l, p<0.001), which was not accompanied by changes in thyroid hormones. Mean baseline NOx levels were 12.6+/-1.2 micromoles/l and showed a significant increase on day 3 (20.1+/-1.2 micromoles/l, p<0.05 vs day 0), followed by progressive reduction from day 6 (18.1+/-2.8 micromoles/l) to day 9 (10.6+/-1.3 micromoles/l, p<0.05 vs day 0). There was a significant (p=0.04) correlation between the percentage increase in TSH and the percentage increase in NOx. On the other hand, increase in TSH did not correlate with the percentage decrease in NOx from day 6 to day 9. No correlation was noted between the increase in TSH or NOx and the occurrence or severity of the symptoms. Our study shows that, during rhTSH testing, circulating nitric oxide increases. This endothelial-derived factor might, in turn, mediate the occurrence of vasomotor headache and nausea in some particularly susceptible patients.
 ...
PMID:Circulating nitric oxide is modulated by recombinant human TSH administration during monitoring of thyroid cancer remnant. 1505 71

It has long been known that nitrate and nitrite medications consistently cause significant headache as a side effect. Classical research has shown that cerebral vasodilation accompanies the use of these medications. More modern studies suggest that these vasodilators exert their action on blood vessels via nitric oxide and its second messenger, cyclic guanosine monophosphate. This paper reviews research studies and theoretical articles which address the concept that nitric oxide plays a major role in the vasodilation associated with the headache phase of migraine with aura. A brief discussion of nitric oxide biochemistry and pharmacology follows. In addition, there is a review of evidence examining the possible contributions of nitric oxide to the neurogenic and vascular events associated with spreading cortical depression, an animal model of migraine aura. The paradoxical hypotheses that nitric oxide may contribute to both the propagation of spreading cortical depression and its limitation are presented. Finally, a rationale for the experimental use of nitric oxide agonists and antagonists in the abortion of migraine aura is introduced.
Headache 1999 Feb
PMID:Potential neurogenic and vascular roles of nitric oxide in migraine headache and aura. 1561 4

Pentaerythritol tetranitrate (PETN) has raised a great deal of interest in recent years, because it is probably the only organic "tolerance-sparing" nitrate. However, some clinicians doubt whether this drug is really effective in reducing angina and ischemia. The aim of this study, therefore, was to evaluate the clinical efficacy and adverse effects (AEs) of PETN in two doses: 50 mg (PETN-50) and 100 mg (PETN-100), after single ingestion. Twenty-five male patients (pts) with stable angina were enrolled in a randomized, double-blind and placebo (P) controlled study. Ten of them received PETN-50 or P and fifteen of them PETN-100 or P. Antianginal efficacy of the drugs was evaluated by analyzing the parameters of tolerance of effort and coronary reserve taken from serial exercise stress tests on the treadmill performed before single oral ingestion, then after 2h and 6h. Simple hemodynamic parameters were also evaluated at rest and during exercise. In comparison to P, PETN-50 did not change any parameter of tolerance of effort and coronary reserve, nor any simple hemodynamic parameter (all values statistically not significant - n.s.). However, in comparison to P, PETN-100 significantly improved the mean total walking time after 2h by 20.8% (p < 0.01) and also after 6h by 11.3% (p < 0.05). Similarly, PETN-100 improved walking time to angina after 2h by 18.8% (p < 0.05) and after 6h by 10.5% (p < 0.05). The drug also improved walking time to ischemia after 2h by 32.5% (p < 0.01) and after 6h by 13.8% (p < 0.05). PETN-100 did not significantly change the resting heart rate, but it decreased resting systolic blood pressure in both positions 6h after ingestion: in supine by 6.1% (p < 0.05) and in standing by 5.9% (p < 0.05). No postural hypotension in any pt occurred. Diastolic blood pressure significantly decreased only in standing position by 6.8% (p < 0.05) after 6h. During maximal exercise no significant reduction of systolic blood pressure occurred, but there was a significant reduction in diastolic blood pressure 6h after ingestion only. This study shows the good clinical tolerance and safety of PETN in both doses. There were no AEs after single ingestion of PETN-50 and AEs after ingestion of PETN-100 included headaches in 3 pts only (in 1 pt after P) in the group of 15 pts. Thus no clinical activity of PETN-50 was shown. However, our investigations suggest that PETN-100 is an active coronary drug, effective not less than 6 h after ingestion, and well tolerated by pts. Further studies are needed to evaluate the efficacy of PETN in long-term therapy.
 ...
PMID:[Clinical evaluation of pentaerythritol tetranitrate in two doses in patients with stable angina pectoris]. 1605 12

Cardiac cephalgia, or headache occurring as manifestation of myocardial ischemia, has only recently been recognized as a distinct entity. In patients with known ischemic cardiopathy, its diagnosis depends on the presence of severe headache that is accompanied by nausea, worsened by physical exercise, and only ceases with nitrate administration. We report on two patients who met diagnostic criteria for this entity. In both, headache was the only symptom of coronary ischemia, and delayed its diagnosis. Headache occurred both at rest and during exertion, and resolved only after the administration of nitrates. Cardiac cephalgia should be suspected in patients with a history of ischemic cardiopathy who present with de novo headache, even when thoracic pain is absent, especially if the headache improves with nitrates. Differential diagnosis with migraine is crucial to avoid the administration of vasoconstrictors.
 ...
PMID:[Cardiac cephalgia: an underdiagnosed condition? ]. 1670 98

Nitrates are very effective antianginal and anti-ischaemic agents. Provision of a long nitrate-free interval or low plasma nitrate levels prior to the morning dose prevents the loss of clinical efficacy by preventing the development of tolerance. However, side effects during nitrate therapy are common. Headache is the most common side effect of nitrates; often dose-related and reported by up to 82% of patients in placebo-controlled trials. Nearly 10% of patients are unable to tolerate nitrates due to disabling headaches or dizziness. In others, headaches are mild-to-moderate in severity and either resolve or diminish in intensity with continued nitrate therapy. Nitrate-induced hypotension is common, but often asymptomatic. In rare instances, nitrate-induced hypotension is severe and accompanied by marked slowing of the heart rate and syncope. Use of nitrates in patients who experience syncope after administration of nitrates is contraindicated. Nitrates rarely cause coronary steal and myocardial ischaemia. Nitrate rebound may occur and patients may experience nocturnal anginal episodes during intermittent therapy with nitroglycerin patches. Administration of nitrates is contraindicated with concomitant use of phosphodiesterase-5 inhibitors used for the treatment of erectile dysfunction, as combination therapy may lead to profound hypotension and even death. There are disturbing observational reports in the literature that continuous, prolonged use of nitrates may lead to increased mortality and recurrent myocardial infarctions. Large, randomised, placebo-controlled studies are needed to confirm or refute these reports; until then, the use of nitrates to treat angina is here to stay.
 ...
PMID:Side effects of using nitrates to treat angina. 1690 56

A new controlled-release isosorbide-5-mononitrate (CR-ISMN) preparation has been developed to meet the requirement for a low nitrate concentration interval in order to avoid nitrate tolerance. We conducted a randomized, double-blind, placebo-controlled study in 31 Japanese patients with stable effort angina pectoris to investigate the efficacy and safety of CR-ISMN. Patients were randomly assigned to either CR-ISMN (40 mg once daily) or placebo groups for 2 weeks after two consecutive symptom-limited treadmill exercise tests using the Bruce protocol to ascertain the reproducibility of exercise tolerance during the placebo run-in period. Exercise tests were repeated at 5, 12, and 24 hours after administration on the final day. No significant difference in exercise time to moderate angina was identified between the CR-ISMN and placebo groups at 5, 12, or 24 hours after administration. However, the changes in exercise were prolonged at 5 hours but not shortened at 24 hours in the CR-ISMN group. The results of subgroup analysis suggested that the concomitant use of insulin might lead to confounding results. Although headache was the most frequent adverse effect in the CR-ISMN group, all symptoms were mild and at self-limiting levels. The plasma concentrations of CR-ISMN maintained therapeutic levels at 5 and 12 hours, and gradually decreased to less than the minimum therapeutic concentration (100 ng/mL) at 24 hours after administration. This study demonstrates that CR-ISMN improves exercise tolerance during the daytime and is well-tolerated in Japanese patients with stable effort angina pectoris without increasing the number of serious adverse effects.
 ...
PMID:Efficacy and safety of controlled-release isosorbide-5-mononitrate in Japanese patients with stable effort angina pectoris. 1710 40

This study evaluated a relationship between nitric oxide (NO) and migraine attacks in order to gain insight into migraine pathomechanism. The study groups consisted of 12 migraineurs and eight controls. All subjects collected morning urine samples for 40 consecutive days. Urinary NO metabolites, nitrite/nitrate (NO(x)) levels were measured with the vanadium-based assay, whilst creatinine (Cr) and neopterin were determined with high-performance liquid chromatography. The mean urinary NO(x)/Cr ratio and number of NO(x) peaks was significantly greater in the migraine group compared with controls (P = 0.01 and P = 0.007, respectively). In the second approach, high NO(x) values were re-assessed in relation to raised neopterin, a marker of systemic infection or inflammation, and were excluded. The excretion of NO(x) persisted being pulsatile, and migraineurs had more peaks compared with controls (P = 0.01). In seven patients, NO(x) peaks coincided with headache days. This was more frequent than expected by random association in four patients (Monte-Carlo simulation; odds ratios: 2.16-7.77; no overlap of 95% CI). In four patients, NO(x) peaks preceded or followed headache days. Although there is a difference in the pattern of urinary NO(x) excretion between control and migraine populations, the variable temporal association of NO(x) peaks and headaches suggests a complex role of NO in this condition.
 ...
PMID:Increased urinary excretion of nitric oxide metabolites in longitudinally monitored migraine patients. 1711 18


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>