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)

Phenylethylamine can initiate migraine-type headaches in susceptible individuals. Migraine sufferers have a reduced ability to deaminate all monoamines, but particularly phenylethylamine. Phenylethylamine readily crosses the blood-brain barrier and thus could be a mediator of the cerebrovascular disturbances seen in migraine attacks. Cerebral blood flow was measured in 15 anesthetized baboons by the intracarotid 133Xe clearance technique. Phenylethylamine (4 x 10(-7) moles.kg-1min-1) produced significant increases in cerebral blood flow (36 percent) and cerebral oxygen consumption (45 percent) during the first 40 minutes of infusion. In contrast, an increased phenylethylamine concentration (2 X 10(-6) moles.kg-1min-1) constricted the cerebral bed (cerebral blood flow reduced by 28 percent). The response of the cerebral circulation to hypercapnia was preserved during the infusion. Phenylethylamine thus is capable of producing in an experimental animal a pattern of cerebrovascular events similar to those seen in migraine.
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PMID:Phenylethylamine and cerebral blood flow. Possible involvement of phenylethylamine in migraine. 40 34

A 25-year-old woman with documented mastocytosis developed hypoxemia with pruritus, diarrhea, headache, and hypotension on two separate occasions. The hypoxemia appeared to be related to a massive release of histamine. Resolution of the patient's symptoms was accompanied by the return of her arterial oxygen tension to normal levels.
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PMID:Respiratory distress and hypoxemia in systemic mastocytosis. 42 34

Three cases of brain abscess following an occlusion of the internal carotid artery were reported. Case 1: A 6-year-old girl with congenital heart disease was admitted with headache, disturbance of consciousness and left hemiparesis. Right carotid angiography revealed an occlusion of the right internal carotid artery. After 6 months, she was readmitted with high fever. CT scan revealed a low density area and a ring-like shadow at the same site of cerebral infarction. Case 2: A 69-year-old man was admitted in semicoma and with right hemiplegia. Left angiography revealed an occlusion of the left internal carotid artery. After 2 months, a brain abscess was noted in the infarcted area. Case 3: A 20-year-old man with congenital heart disease, was admitted due to headache, vomiting and high fever. CT scan revealed a brain abscess in the right frontal lobe. Carotid angiography showed bilateral internal carotid artery occlusion. We concluded that diminution of cerebral oxygen and encephalomalacia are predisposing factors to the evolution of brain abscess.
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PMID:[Brain abscess (Part 5)--Brain abscess following internal carotid occlusion (author's transl)]. 49 56

Guancydine (1-cyano-3-tert-amylguanidine) lowered within normal limits the tensional values in an interval of four hours after its administration in eight out of nine hypertensive patients under experiment. The hypotensive effect of a single oral dose of 500-750 mg persists for about 6-7 hours after its administration. Guancydine does not impair the vasopressor response to angiotensin II but reduces the action of this peptide on the excretion of water, Na, K and Ca through urine. The hypotensive effect of Guancydine is associated with a decrease of platelet adhesiveness and an activation of fibrinolysis. In view of this fact, Guancydine might play a role in the prophylaxis of complications of arterial hypertension - atherosclerosis and trombosis. The increase of venous blood oxygenation after Guancydine could be attributed to the opening of arterio-venous shunts or to the reduction of tissular extraction of oxygen. Guancydine does not seem to be toxic. It produced, in some patients, slight headache and orthostatic hypotension, especially during the first hours after administration.
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PMID:Guancydine, a new hypotensive agent with complex action. 56 30

Twenty-two smokers with elevated hematocrits (mean, 54 per cent) had elevated blood carboxyhemoglobin (mean, 11.6 per cent; normal, less than 1 per cent) and a "left-shifted" oxygen-hemoglobin dissociation curve (mean P50, 21.6 +/- 2.3 [+/- S.D.] torr; normal, 26.7 +/- 1.1). Red-cell volume was increased in 14 of 18, and plasma volume reduced in 14 of 18. Fatigue and headache were common, and syncopal attacks occurred in four patients. Symptoms disappeared and the elevated red-cell volume decreased markedly in all five patients who were able to reduce severely their smoking habit; low plasma volume increased in three of four patients studied. We conclude that carbon monoxide exposure from cigar and cigarette smoke is a frequent cause of an elevated red-cell volume or a reduced plasma volume (or both). Measurement of carboxyhemoglobin should be a routine part of the evaluation of all polycythemic subjects.
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PMID:Smokers' polycythemia. 61 65

In two siblings with limb-girdle muscle weakness and episodic headaches and vomiting from early childhood, progressive neurologic degeneration later developed, and both children died. In one child, corticosteroids induced improvement in both cerebral and muscular symptoms that lasted 1 year. This patient had elevated blood, urine, and spinal fluid lactate levels, together with increased cardiac output and oxygen consumption at rest. Several muscle fibers were characterized by a "ragged red" appearance with the trichrome stain. Subsarcolemmal and intermyofibrillar excess of mitochondrial oxidative enzyme reaction product was correlated with abnormal mitochondrial aggregates by electron microscopy. The brain revealed focal areas of cortical degeneration and necrosis with adjacent gliosis or edema. Ferrocalcific deposits were prominent in the globus pallidus. The other sibling had similar changes in the brain at autopsy. This familial multisystem disorder especially involving the brain, skeletal muscle, and heart appears to represent a defect in some mitochondrial oxidative mechanism.
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PMID:Familial poliodystrophy, mitochondrial myopathy, and lactate acidemia. 117 91

Nicorandil is a new vasodilator agent. Efficacy and safety of nicorandil in the treatment of angina pectoris have been evaluated through an extensive clinical program with a total of 1,680 patients who received the product. Results of hemodynamic studies provide clear evidence of the vasodilatory effect of nicorandil. In a population of patients with normal left ventricular function, a reduction in preload was apparent from a decrease in left ventricular end-diastolic pressure from 7.4 +/- 1.7 to -3.2 +/- 1.5 mm Hg. Furthermore, nicorandil produced marked reductions in total peripheral resistance (19%) and aortic blood pressures with decreases in systolic pressure of 34% and in diastolic pressure of 21%. At antianginal doses, nicorandil has a coronary vasodilating effect as well as a balanced peripheral action that leads to decreases in both preload and afterload. Therefore, nicorandil affects two of the main hemodynamic determinants of oxygen demand without impairing myocardial contractility or atrioventricular conduction. In addition, its strong spasmolytic activity is of particular interest when dynamic coronary obstruction is considered. Nicorandil clearly has demonstrated K(+)-channel-opening activity. In addition, the range of plasma concentrations in humans at therapeutic doses is similar to that of experimental models in which the K(+)-channel activity has been determined. This mechanism of action may explain the different hemodynamic profiles of nicorandil and nitrates in humans. Nicorandil is an effective and potent antianginal agent at a dose of 10-40 mg, which in monotherapy controls 69-80% of patients with stable chronic angina. Comparative trials have shown that the efficacy of nicorandil compares with that of drugs from the main classes of antianginal drugs--beta-blockers (atenolol, propranolol) and a Ca2+ antagonist (diltiazem). Patients treated for as long as 3 months or 1 year have shown sustained efficacy with no evidence of development of tolerance to the drug. The long duration of action allows effective treatment with a well-tolerated b.i.d. regimen. At the recommended doses, the main side effects were limited to headaches. They usually occurred early in the course of treatment and can be diminished by a progressive titration. From the large safety data base, there is no evidence that nicorandil induced exacerbation of myocardial ischemia or abrupt withdrawal syndrome. Nicorandil does not adversely affect the lipid profile or the glucose level. As an antianginal drug with a novel mechanism of action, nicorandil provides a useful alternative to existing antianginal agents in the long-term management of patients with angina pectoris.
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PMID:Clinical profile of nicorandil: an overview of its hemodynamic properties and therapeutic efficacy. 128 84

In a double-blind, placebo-controlled trial, human brain function and mental performance were studied under two different degrees of hypoxia after administration of two different doses (6 mg and 9 mg) of co-dergocrine mesylate (CDM) utilizing blood gas analysis, EEG mapping and psychometry. Hypoxic hypoxidosis (i.e. impairment of cerebral metabolism due to hypoxia) was experimentally induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) (found in 6000 m altitude), and of 8.6% O2, 91.4% N2 (found in 7000 m altitude), which was inhaled for 23 min under normobaric conditions by 18 healthy volunteers. They received randomized after an adaptation session placebo, 6 mg and 9 mg co-dergocrine mesylate (CDM). Evaluation of blood gases, brain mapping and psychometry was carried out at 0, 2, 4, 6, 8 h after oral drug administration. Blood gas analysis demonstrated a drop in PO2 to 42 and 32 mm Hg 23 min after inhalation of the 9.8% and 8.6% gas mixture, respectively, PCO2 decreased to 32 and 31 mm Hg, pH increased to 7.46 and 7.47 and base excess increased to 0.50 and 0.90 nmol/l, respectively. EEG mapping demonstrated an increase in delta and decrease of alpha power and a slowing of the centroid over almost the whole brain. 6 mg and slightly less so 9 mg CDM attenuated this deterioration of vigilance (i.e. dynamic state of the neuronal network determining adaptive behavior). At the behavioral level, moderate hypoxia induced a deterioration of noopsychic performance, which was mitigated by 6 mg, but not by 9 mg CDM. A deepening of the hypoxia resulted in a loss of these brain protective effects of both doses. Decrement of the thymopsyche increased after both doses in the moderate hypoxic condition, while under marked hypoxia 6 mg CDM attenuated and 9 mg aggravated this deterioration. Time-wise, brain protective effects reached the level of statistical difference between the 2nd and the 6th hour. Somatic complaints like feeling dazed, giddiness and headache were mitigated dose dependently by CDM in the moderate, but not in the marked hypoxic hypoxidosis.
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PMID:Dose-response studies with co-dergocrine mesylate under hypoxia utilizing EEG mapping and psychometry. 136 69

Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & Therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.
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PMID:Management of the moribund carbon monoxide victim. 811 Mar 42

Nocturnal oxygen desaturation (NOD) is commonly seen not only in sleep apnea syndrome (SAS) but also in chronic lung disease (CLD) including chronic obstructive lung disease even without sleep apnea. However, the relationship of NOD to clinical symptoms such as morning headache, sleep deprivation due to breathlessness, and daytime sleepiness is not known. In this study, we examined by polysomnography the relationship between several NOD indexes, parameters of apnea, and subjective symptoms in 25 patients with SAS and 22 patients with CLD. In addition, the relation between daytime arterial blood gas data and NOD indexes, parameters of apnea, was examined. In the SAS group, there were no differences in any parameters of NOD and apnea between patients with subjective symptoms and those without symptoms. However, in the CLD group, symptomatic patients had significantly lower lowest SaO2, higher mean SaO2, and longer total desaturation time. In both groups, daytime PaCO2 had a significant correlation with several NOD parameters such as mean SaO2, lowest SaO2, and total desaturation time. In the SAS group, daytime PaCO2 was also correlated with the parameters of apnea. On the other hand, daytime PaO2 was significantly correlated with mean SaO2 only in the CLD group. From these data, we conclude that in patients with SAS, daytime PaCO2 is a variable that is related to the degree of NOD, and that in patients with CLD, subjective symptoms and daytime PaO2 in addition to daytime PaCO2 are associated with NOD.
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PMID:[Relationship between clinical symptoms and nocturnal oxygen desaturation in sleep apnea syndrome and chronic lung disease]. 140 71


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