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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of the available literature concerning sudden withdrawal of antihypertensive drugs shows that withdrawal syndromes after cessation of such agents have occurred with beta-blockers, methyldopa, clonidine hydrochloride, guanabenz, and bethanidine sulfate. Most commonly, these syndromes are limited to nervousness, tachycardia, headache, and nausea 36 to 72 hours after cessation of the drug. In rare cases, serious exacerbation of myocardial ischemia (beta-blockers) or hypertension (clonidine, methyldopa) may occur in the posttreatment period. The withdrawal syndromes generally respond promptly to reinstitution of antihypertensive therapy. The infrequent occurrence of withdrawal syndromes should not discourage use of these efficacious agents.
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PMID:Withdrawal syndromes and the cessation of antihypertensive therapy. 611 20

The antiarrhythmic efficacy and safety of oral flecainide acetate and quinidine sulfate were compared in a double-blind, 16-center parallel trial involving 280 patients with chronic premature ventricular complexes (PVCs). Eighty-five percent of the flecainide patients had at least 80% suppression of PVCs, vs 57% of the quinidine patients (p less than 0.0001). Sixty-eight percent of the flecainide patients met the above criterion and also had complete suppression of couplets and beats of ventricular tachycardia, vs 33% of the quinidine patients (p less than 0.0001). PR and QRS intervals were prolonged by flecainide without clinical consequence, but they were not substantially affected by quinidine (p less than 0.0001). Quinidine prolonged JT (QT minus QRS) intervals significantly more than flecainide (p less than 0.05). Nineteen of 141 flecainide patients and 21 of 139 quinidine patients discontinued therapy because of side effects (p greater than 0.50). Flecainide side effects included dizziness, blurred vision, headache and nausea. Quinidine side effects included diarrhea, nausea, headache and dizziness. Flecainide was more effective than quinidine in suppressing chronic ventricular arrhythmias (especially complex forms), and thus is an important new antiarrhythmic agent.
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PMID:Flecainide versus quinidine for treatment of chronic ventricular arrhythmias. A multicenter clinical trial. 633 10

Eclampsia occurring more than 48 hours postpartum has been observed in an unusual number of patients. From August 1977 to November 1982 at E. H. Crump Women's Hospital and Perinatal Center (Memphis), there were 132 documented cases of eclampsia, of which 36 (27%) occurred postpartum. Seventeen (47%) of these occurred more than 48 hours postpartum. Preeclampsia was diagnosed before the onset of convulsions in 12 patients, all of whom received intravenous magnesium sulfate postpartum. The mean duration of postdelivery magnesium sulfate therapy was 32 hours (range 24 to 72 hours). Headaches and visual disturbances were reported by all 17 patients before onset of convulsions. Physical and laboratory findings immediately after the convulsions were consistent with eclampsia. Treatment consisted primarily of intravenous magnesium sulfate. Neurologic consultation was obtained to rule out a neurologic disorder, and metabolic studies were also done. Electroencephalograms were done on 15 patients; eight of them showed patterns consistent with encephalopathy.
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PMID:Late postpartum eclampsia: an update. 664 9

Dural sinus thrombosis developed in two children with acute lymphoblastic leukemia during induction treatment with vincristine sulfate, prednisone, and asparaginase. Headache, nausea, emesis, and lethargy were the presenting signs. The diagnosis was confirmed by arteriography. The cause is presumed to be secondary to hypercoagulability due to asparaginase-induced antithrombin III deficiency. The patients received anticoagulation therapy and recovered completely. Only two of the six reported patients without heparinization survived.
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PMID:Dural sinus thrombosis in children with acute lymphoblastic leukemia. 694 95

In a double-blind dose response study in 26 children, 3, 6, or 12 microgram/kg of terbutaline sulfate was compared with 10 microgram/kg of epinephrine administered subcutaneously. In the first hour after injection, all doses of terbutaline and epinephrine resulted in improvement in mean clinical score, mean forced vital capacity, mean forced expiratory volume in the first second, and mean forced expiratory flow from 25% to 75% of vital capacity. Terbutaline epinephrine. However, while adverse effects following terbutaline were clinically imperceptible, epinephrine produced unpleasant headache and excitement in a few patients. Terbutaline did not change mean PaO2 or PaCO2 significantly in a subgroup of patients. The 12 microgram/kg dose of terbutaline was superior to 3 or 6 microgram/kg in relieving obstruction to airflow measured at the midportion of the vital capacity. This dose caused tremor in some children, but the tremor was not apparent to patients or their parents.
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PMID:Dose response of subcutaneous terbutaline and epinephrine in children with acute asthma. 721 75

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

Mortality of 70% of all patients with tumors in the head and neck is linked with anorexia and cachexia. Two reasons for cachexia are well known: 1. local disease and local therapy preventing oral nutrition and 2. advanced tumors activating biochemical pathways of proteolysis, lipolysis, and gluconeogenesis. Five groups of substances are now used to treat tumor-induced cachexia: corticosteroids, progestational drugs, cyproheptadine, hydrazine sulfate, and anabolic steroids. Between 1992 and 1993 we treated 38 patients suffering from cachexia due to advanced cancers of the head and neck with 160 mg megestrol acetate per day for four months. The increase in body weight was significant after eight weeks. The mean increase after full therapy was 4.58 +/- 3.19 kg. Treatment of the five women in the series was very successful and all achieved their former body weight. Megestrol acetate therapy was best started after assuring enteral nutrition. Significant adverse events were loss of libido for the men, headache and, rarely, thrombophlebitis. Our first experiences suggest that megestrol acetate treatment is useful in cachectic patients with advanced squamous cell carcinomas of the head and neck.
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PMID:[Value of megestrol acetate in treatment of cachexia in head-neck tumors]. 757 3

Molybdenum is found in most foods, with legumes, dairy products, and meats being the richest sources. This metal is considered essential because it is part of a complex called molybdenum cofactor that is required for the three mammalian enzymes xanthine oxidase (XO), aldehyde oxidase (AO), and sulfite oxidase (SO). XO participates in the metabolism of purines, AO catalyzes the conversion of aldehydes to acids, and SO is involved in the metabolism of sulfur-containing amino acids. Molybdenum deficiency is not found in free-living humans, but deficiency is reported in a patient receiving prolonged total parenteral nutrition with clinical signs characterized by tachycardia, headache, mental disturbances, and coma. The biochemical abnormalities in this acquired molybdenum deficiency include very low levels of uric acid in serum and urine (low XO activity) and low inorganic sulfate levels in urine (low SO activity). Inborn errors of isolated deficiencies of XO, SO, and molybdenum cofactor are described. Although XO deficiency is relatively benign, patients with isolated deficiencies of SO or molybdenum cofactor exhibit mental retardation, neurologic problems, and ocular lens dislocation. These abnormalities seem to be caused by the toxicity of sulfite and/or inadequate amounts of inorganic sulfate available for the formation of sulfated compounds present in the brain. XO and AO may also participate in the inactivation of some toxic substances, inasmuch as studies suggest that molybdenum deficiency is a factor in the higher incidence of esophageal cancer in populations consuming food grown in molybdenum-poor soil.
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PMID:Molybdenum: an essential trace element. 830 61

Patients with cluster headaches have been reported to have low serum ionized magnesium levels. We examined the possibility that patients with cluster headaches and low ionized magnesium levels may respond to an intravenous infusion of magnesium sulfate. Thirty-eight infusions of magnesium sulfate were given to 22 patients with cluster headaches. The mean ionized magnesium level prior to 23 infusions which provided relief for at least 2 days and enabled the patient to skip two or more attacks, was 0.521 +/- 0.016 mmol/L; this value was 0.561 +/- 0.016 prior to 15 infusions which were ineffective. These latter 15 infusions were preceded by higher total magnesium levels. The ionized magnesium level prior to the 23 effective infusions was below 0.54 mmol/L in 19 patients. Five of the 15 ineffective infusions were accompanied by basal ionized magnesium levels below 0.54 mmol/L. In 76% of the infusions, there was a correlation between a response and an ionized magnesium level below 0.54 mmol/L. Nine patients (41%) obtained clinically meaningful improvement. Spontaneous remissions and a placebo effect might have accounted for some of the improvement. However, this should have applied equally to all patients, regardless of the ionized magnesium level. Measurements of ionized magnesium may prove useful in elucidating the pathogenesis of cluster headache and in identifying patients who may benefit from treatment with magnesium.
Headache
PMID:Intravenous magnesium sulfate relieves cluster headaches in patients with low serum ionized magnesium levels. 855 Mar 60

This study was designed to investigate tyramine sulfate conjugation in patients with migraine or tension-type headache, as defined by the newly introduced International Headache Society (IHS) criteria and to examine whether this relationship is mediated by major depression. A total of 62 subjects completed the study: 38 with migraine (22 with aura and 16 without aura), 12 with tension-type headache, and 12 controls. Patients with migraine had significantly lower urinary tyramine sulfate excretion following oral tyramine challenge than normal control. Tension-type headache was also associated with low tyramine conjugation, but only when comorbid with depression. Although mean tyramine sulfate output was lower among subjects with major depression within each of the subtypes of headache, no significant main effect emerged for depression or major subtype thereof. The lower tyramine sulfate excretion values among patients with both migraine and depression compared to those of migraine alone or depression alone in our data and those of others suggests that comorbid migraine with depression may represent a more severe form of migraine than migraine alone. The findings underscore the importance of comorbidity in clinical and epidemiological studies of migraine.
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PMID:Tyramine conjugation deficit in migraine, tension-type headache, and depression. 858 Feb 25


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