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)

Sumatriptan, a 5-hydroxytryptamine1, (5-HT1) receptor agonist is an effective abortive agent for migraine headaches. A common side effect in 3% to 7.9% of patients is chest pain. Although most cases of chest pain are not thought to be of cardiac origin, its mechanism is not entirely understood. Rare examples of electrocardiogram changes consistent with transient ischemia have been reported. Isolated instances of angina, arrhythmia, myocardial infarction, and death have been temporally associated with sumatriptan administration. In most cases, it is unclear whether underlying cardiovascular disease existed or contributed to this adverse event. We report the history of a 56-year-old female patient with migraine who experienced a myocardial infarction shortly after using sumatriptan, despite having had a normal cardiovascular evaluation. As she had a normal cardiac catheterization after the event, we find it probable that sumatriptan induced coronary vasospasm and myocardial infarction.
Headache 1996 May
PMID:Vasospasm-induced myocardial infarction with sumatriptan. 868 77

The rupture of a cerebral aneurysm is the main cause of a spontaneous subarachnoid hemorrhage. Complications after the initial hemorrhage are recurrent bleeds, hydrocephalus and ischemia. Main symptom of a subarachnoid hemorrhage is the sudden, intense headache, often followed by loss of consciousness. The diagnosis is made by CT. If the CT is negative, lumbar puncture has to be performed, because in 5% of patients the blood may not be seen on the CT. If the diagnosis is confirmed, the patients has to be transferred as an emergency to a neurosurgical center. If his condition is satisfactory, the aim of the treatment is to occlude the ruptured aneurysm by microsurgical technique within the first three days after the hemorrhage. In patients with high surgical risk or bad general condition, the aneurysm can also be treated by the interventional neuroradiologist with endovascular techniques.
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PMID:[Subarachnoid hemorrhage]. 871 34

Previous studies have shown that migraine with aura is associated with the reduction of regional cerebral blood flow (rCBF). However, the question of whether the reduction of rCBF during migraine aura is caused by cerebral vasospasm or is secondary to the neural depression (spreading depression) is still disputed. We measured rCBF by high resolution SPECT method during the attack of migraine and examined whether the reduction in flow corresponds to the cerebral vascular territory. Fourteen patients with migraine with aura (7 men and 7 women, 34.7 +/- 17.8 years) were studied. In all the patients rCBF was measured during the interictal period and in four patients rCBF was measured during the aura of migraine. SPECT measurements of rCBF was performed using Tc-99m-PAO (740 MBq) as a tracer. During the aura of scintillation scotoma in the unilateral visual field rCBF was reduced in the opposite occipital, temporal and thalamic regions which corresponded clearly to the region of the posterior cerebral arterial territory. The reduction of rCBF was by 31 approximately 49% compared with the opposite hemisphere. Cerebral spinal fluid lactate level during the headache measured in one patient was higher (38 mg/dl) than the interictal period (12 mg/dl). Our data indicated that the reduction of rCBF during the aura is caused by ischemia probably due to the cerebral vasospasm and is not secondary to the neuronal depression. It was also suggested that the primary site of rCBF reduction during the visual aura is the occipital association cortex which is reported to be responsible for the visual hallucination.
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PMID:[Regional cerebral blood flow during migraine]. 875 89

Magnesium ions (Mg2+) are pivotal in the transfer, storage and utilization of energy; Mg2+ regulates and catalyzes some 300-odd enzyme systems in mammals. The intracellular level of free Mg2+ ([Mg2+]i) regulates intermediary metabolism, DNA and RNA synthesis and structure, cell growth, reproduction, and membrane structure. Mg2+ has numerous physiological roles among which are control of neuronal activity, cardiac excitability, neuromuscular transmission, muscular contraction, vasomotor tone, blood pressure and peripheral blood flow. Mg2+ modulates and controls cell Ca2+ entry and Ca2+ release from sarcoplasmic and endoplasmic reticular membranes. Since the turn of this century, there has been a steady and progressive decline of dietary Mg intake to where much of the Western World population is ingesting less than an optimum RDA. Geographic regions low in soil and water Mg demonstrate increased cardiovascular morbidity and mortality. Dietary deficiency of Mg2+ results in loss of cellular K+ and gain of cellular Na+ and calcium ions (Ca2+). Blood normally contains Mg2+ bound to proteins, Mg2+ complexed to small anion ligands and free ionized Mg2+ (IMg2+). Most clinical laboratories only now assess the total Mg, which consists of all three Mg fractions. Estimation of the IMg2+ level in serum or plasma by analysis of ultrafiltrates (complexed Mg + IMg2+) is somewhat unsatisfactory, as the methods employed do not distinguish the truly ionized form from Mg2+ bound to organic and inorganic anions. Because the levels of these ligands can vary significantly in numerous pathological states, it is desirable to directly measure the levels of IMg2+ in complex matrices such as whole blood, plasma and serum. Using novel ion selective electrodes (ISE's), we have found that there is virtually no difference in IMg2+, irrespective of whether one samples whole blood, plasma or serum. These data demonstrate that the mean concentration of IMg2+ in blood is about 600 mumoles/litre (0.54-0.65 mmol/L, 95% Cl); 65-72% of total Mg being free or biologically-active Mg2+. Use of the NOVA and KONE ISE's for IMg2+ on plasma and sera from patients with a variety of pathophysiologic and disease syndromes (e.g., long-term renal transplants, liver transplants, during and before cardiac surgery, ischemic heart disease [IHD], headaches, pregnancy, neonatal period, non-insulin dependent diabetes (NIDDM), end-stage renal disease [ESRD], hemodialyse [HEM], and continuous ambulatory peritoneal dialysis (CAPD), hypertension, myocardial infarction [AMI] and after excessive dietary intake of Mg), has revealed interesting data. The results indicate that long-term renal transplant patients, headache, pregnant, NIDDM, ESRD, HEM, CAPD, AMI, hypertensive, and IHD subjects exhibit, on the average significant depression in IMg2+ but not TMg. Use of 31P-NMR spectroscopy on red blood cells, from several of these disease states, to assess free intracellular Mg ([Mg2+]i demonstrates a high correlation (r = 0.5-0.8) between IMg2+ and [Mg2+]i. Increased dietary load of Mg, for only 6 days, in human volunteers, resulted in significant elevations in serum IMg2+ but not TMg. Correlations between the clinical course of several of the above disease syndromes and the fall in IMg2+ and [Mg2+]i were found. The ICa2+/IMg2+ ratio appears, from our data, to be an important guide for signs of peripheral vasoconstriction, ischemia or spasm and possibly atherogenesis. Overall, our data point to important uses for ISE's for IMg2+ in the diagnosis and treatment of disease states.
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PMID:Role of magnesium in patho-physiological processes and the clinical utility of magnesium ion selective electrodes. 886 38

The first case of a child with an arteriovenous malformation (AVM) associated with moyamoya disease is reported. The patient presented ischemic symptoms and underwent indirect bypass surgery on both sides when she was 5 years old. Four years later she suffered from headache, and a small AVM of the left frontal lobe associated with the moyamoya vessels was detected. Single photon emission computed tomography (SPECT) was performed at age 11 and demonstrated low local cerebral blood flow (CBF) in the left frontal lobe and right temporal lobe, although the revascularization after the bypass surgery seemed to be effective, as judged on pancerebral angiography. We feel that brain ischemia due to the moyamoya disease may have played a causative role in the development of the AVM.
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PMID:Arteriovenous malformation associated with moyamoya disease. 929 67

Ergotamine tartrate (ET) and dihydroergotamine mesylate (DHE) have been widely and effectively used in the treatment of migraine for many decades, although few randomized, controlled clinical trials have been conducted with these compounds. To compare their safety profiles, the world literature on the two agents was surveyed. The results are summarized, along with a critical analysis of the strengths and limitations of the various sources of safety data (in vitro research, animal studies, Phase I and II studies, controlled clinical trials, and postmarketing surveillance). Significant pharmacologic and safety differences exist between ET and DHE. Dihydroergotamine mesylate is a less potent arterial vasoconstrictor than ET, although nearly equipotent as a venoconstrictor. It is a more potent alpha-adrenergic antagonist, but is much less emetic, has less effect on the uterus, and is not associated with rebound headache. Adverse effects associated with ET (which are often due to excessive dosage and/or chronic usage) include nausea, acroparesthesia, ischemia, habituation and overuse headache, and, rarely, overt ergotism. Reports of serious adverse effects following recommended doses of DHE are rare. As with most antimigraine drugs, the most frequent adverse effect with intravenous (i.v.) DHE is nausea; however, following intramuscular (i.m.) or intranasal (IN) administration, the incidence of nausea is low and concomitant administration of an antiemetic is not needed. In patients without contraindications, both DHE and ET are safe and effective when used in recommended doses. Nearly 50 years of clinical experience without major safety problems allows a high level of confidence in their clinical use.
Headache 1997
PMID:Ergotamine tartrate and dihydroergotamine mesylate: safety profiles. 900 72

Midaortic syndrome (MAS) is a well-recognized but rare cause of renovascular hypertension (RVH). Several techniques have been described to treat RVH caused by MAS. The authors recently treated two children with MAS and RVH. In both patients the right kidney had two renal arteries. A 13-year-old boy presented with severe headaches, pain in his lower extremities with exertion, and marked hypertension (blood pressure, 170/110). An aortogram demonstrated 70% narrowing of his abdominal aorta from the suprarenal region to 5 cm above the iliac bifurcation. There was significant stenosis of the celiac axis, superior mesenteric artery, and left renal artery. The right kidney had two renal arteries, and the upper pole artery was stenotic at its origin. A 10-year-old girl, known to have hypertension for several years had an aortogram that demonstrated 70% narrowing of the abdominal aorta from the suprarenal region to 3 cm above the iliac bifurcation. There was involvement of the left renal artery at its orifice. She also had two renal arteries to the right kidney with the right upper pole artery being stenotic at its origin and in the mid-portion of the vessel. Aortic reconstruction was accomplished with a polytetrafluoroehtylene (PTFE) bypass graft in each case. The first case also involved patch angioplasty of the celiac axis. In both cases, the right kidney was autotransplanted. It was removed intraoperatively, cold perfused, and the two renal arteries reconstructed followed by transplantation to the right iliac vessels. In both cases the left renal artery was reimplanted into the PTFE graft. Both patients had uncomplicated postoperative courses. The 13-year-old boy had evidence of renal ischemia in a portion of the lower pole of the autotransplanted kidney by DTPA scan. He has mild hypertension controlled with antihypertensive medication. The 10-year-old girl has a normal DTPA scan and is normotensive. MAS is a rare and challenging congenital vascular anomaly that causes RVH. In the presence of double renal arteries the technique of autotransplantation with cold perfusion and "bench" vascular reconstruction reduces the warm ischemia time and should produce satisfactory results.
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PMID:Renal autotransplantation for renovascular hypertension caused by midaortic syndrome. 904 31

Vestibular symptoms frequently occur in patients with migraine headache. The common migraine is defined in neurology as a unilateral, pulsating headache, which may be associated with nausea and vomiting, and lasts one or several days. In the classic form patients have visual prodromal symptoms. Focal neurological signs in the migraine complique include, for example, oculomotor palsy and vestibular abnormalities. This so-called vestibular migraine is different from basilar migraine, which involves the irritation of the cervical sympathetic system, and can cause symptoms that resemble transient brainstem ischemia. In order to evaluate vestibular dysfunction electronystagmography (ENG) was used. Patients frequently had abnormal caloric test responses, especially with a directional preponderance, and most had a spontaneous nystagmus. In the migraine attack the patients are presumed to have hypersensitivity of the labyrinth with nausea and vomiting, while in the headache-free period the ENG was almost normal. At present, we have had a high success rate in treating patients with pyracetam. Diazepam was used to treat basilar migraine and flunarizine to prevent vestibular migraine.
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PMID:Vestibular disorders in patients with migraine. 906 28

The authors report two cases of a particular type of migraine with aura, known as familial hemiplegic migraine (FHM). According to the International Headache Society (IHS) diagnostic criteria, the FHM can be diagnosed with the exception of organic causes, in a patient with migraine with aura including emiparesis of anything severity and with an end occurring a member of the family with similarity in the attach pattern. The two clinical cases reported clearly show these features and they can be considered exemplary for this type of pathology. This rare type of migraine has an unknown etiology, it seems to depend on a decreases of cerebral blood flow originative on the occipital lobe, over the subsequentially spreading anteriory region temporal and parietal lobe. The hypoperfusion with the next following neural ischemia is related to the variation of blood flow and/or "the spreading depression" supported by Leao and Olesen recently. We wanted to show these two cases so that the psychiatrist, the pediatrician, and the neurologist can be able to refer parents to the right approach, considering possibility of a pathology rare but benign; this is the FHM.
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PMID:Familial hemiplegic migraine in developmental age: report of two cases. 917 12

Neurologic and visual symptoms frequently occurred in 56 reported patients with essential thrombocythemia (ET). They may either precede or follow the well-known microcirculatory complications of ET of acroparesthesias, erythromelalgia, and acrocyanosis or ischemia of one or more toes. In comparison with transient ischemic attacks in patients with vascular risk factors, the usual neurologic presentation of ET consists of brief attacks of sudden cerebral or visual dysfunction, which can be either well localized or diffuse and entirely nonspecific. A dull and throbby headache usually lasting for several hours frequently accompanies the neurologic symptoms. Visual symptoms are less frequent and include transient monocular blindness and global symptoms such as scintillating scotomas and attacks of blurred vision. Neurologic and visual symptoms may leave minor sequelae but are generally nondisabling. The striking similarity to migraine, together with the absence of vascular risk factors and the striking efficacy of aspirin treatment supports the hypothesis that the ischemic neurologic and visual symptoms in ET are caused by shear rate-induced intravascular activation and aggregation of platelets with subsequent transient sludging or occlusion of the cerebral arterial microvasculature. Available data show that both the erythromelalgic distress and the ischemic neurologic attacks in ET are completely abolished by control of platelet function with low dose aspirin alone or reduction of platelet counts to normal as well as by the combination of platelet reducing therapy and low-dose aspirin. Early recognition and appropriate treatment of neurologic symptoms in patients with ET is therefore of great clinical relevance.
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PMID:Neurologic and visual symptoms in essential thrombocythemia: efficacy of low-dose aspirin. 926 53


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