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

Seventy patients with classical or common migraine were treated during their attacks with either naproxen sodium or placebo in a randomised, double-blind parallel group study. The initial dose of naproxen sodium was 825 mg followed one hour later by a further 550 mg, if symptoms were the same or had improved. If the migraine symptoms had worsened, patients were offered an escape analgesic combination of 1000 mg paracetamol and 10 mg metoclopramide. Patients were assessed at monthly intervals for changes in the severity and duration of headache, premonitory symptoms (mainly visual disturbances) and photophobia, nausea and vomiting associated with migraine attacks that had occurred since the previous visit. Patients were studied for a maximum of ten attacks and significant improvement was observed in the severity and duration of headache when the patients were on naproxen sodium. Also the premonitory symptoms and photophobia improved significantly on naproxen sodium and significantly less rescue analgesics were required. Patients suffering from common migraine had less severe headaches and photophobia when taking naproxen sodium than when taking placebo and the headaches were shorter in duration and patients took less rescue analgesic. No significant difference was observed between the treatment groups in patients with classical migraine. Ten patients in the placebo group and six in the naproxen sodium group reported side-effects but these were possibly related to the use of rescue medication. Naproxen sodium proved safe and effective in common migraine attacks, but in this study efficacy was not established for classical migraine.
Cephalalgia 1985 Mar
PMID:Naproxen sodium in the treatment of migraine. 388 54

The efficacy of safety of naproxen sodium and ergotamine tartrate were compared for the treatment of acute migraine attack in a randomized, parallel trial with 114 participating patients. At the start of symptoms, patients took either three tablets of naproxen sodium (275 mg each) or one of an ergotamine combination (containing 2 mg ergotamine tartrate, 91.5 mg caffeine, and 50 mg cyclizine chlorhydrate). Patients were followed for three months or until six attacks were monitored, whichever came first. Both medications substantially shortened the duration of migraine attacks and reduced the severity of symptoms. When the test medications were taken within 2 h of onset of attack, naproxen sodium was statistically significantly more effective than the ergotamine combination in reducing the severity of headache pain, nausea, and lightheadedness. The ergotamine combination was associated with significantly more vomiting, need for rescue medication, and side effects than was naproxen sodium. Four patients required discontinuation of the ergotamine combination and one of naproxen sodium. Both patients and investigators rated tolerance for naproxen sodium as superior to tolerance for the ergotamine combination. Naproxen sodium seems to be an effective and safe treatment for migraine attacks.
Cephalalgia 1985 Jun
PMID:Acute migraine attack therapy: comparison of naproxen sodium and an ergotamine tartrate compound. 392 22

A 37-year-old woman undergoing endocrine evaluation during her seventh pregnancy because of headaches, weakness, and hyponatremia was found to have central hypoadrenalism and hypothyroidism. Computed tomography showed a pituitary mass with suprasellar extension but her visual fields were intact. She was treated conservatively with hydrocortisone acetate and levothyroxine sodium until 38 weeks of gestation, when healthy twins were delivered by cesarean section. A few months later, her pituitary function improved, with a significant increase in the adrenocorticotropic hormone level, normal values of basal thyroid-stimulating hormone, growth hormone, and gonadotropins and of their functional reserves, and only a slight elevation in the prolactin level. A repeated computed tomographic scan showed disappearance of the pituitary mass.
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PMID:Spontaneous postpartum regression of pituitary mass with return of function. 394 2

The effects of high sodium 144 mmol/l (mEq/l) dialysate were studied in normotensive, hypertensive and anephric chronic hemodialysis patients. Comparisons of blood pressures, weights and side effects associated with the hemodialysis procedure were made between two 6-month periods using dialysate sodium concentration of 133 mmol/l (mEq/l), followed by a high dialysate sodium of 144 mmol/l (mEq/l), each patient acting as his own control. No difference was found in the frequency of cramps or 'disequilibrium' side effects (nausea, vomiting, headache, restlessness). High sodium dialysate is beneficial for normotensive and anephric patients in reducing dialysis-induced hypotension and was not associated with any deleterious effects on long-term blood pressure control. In hypertensive patients, the benefit is less clear, and hypertension may increase.
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PMID:Effects of high sodium dialysate during maintenance hemodialysis. 403 43

A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache, generalized convulsions and progressive disturbance of consciousness. He developed deep vein thrombosis in his right leg and pulmonary emboli two years earlier when he was placed on heparin and so forth, followed by warfarin sodium. Warfarin was terminated 9 months prior to his recent illness. On neurological examination on admission, he was semicomatous with blurred disc margins, roving eye movements with right abducens nerve palsy, nuchal stiffness and right flaccid hemiplegia. Left carotid angiogram and CT scan revealed extensive superior sagittal sinus thrombosis, complicated with hemorrhagic infarcts in bilateral frontal lobes. When examined for coagulation studies, the patient and his father had decrease in AT III activity and antigen levels. He was treated successfully with antiedematous agents and anticonvulsants during acute phase of illness. He was thereafter placed on warfarin 5-6 mg/day with no further clinical thromboembolic event for 2 years 9 months. There was no neurological abnormality when he was last examined, although he was treated with valproic acid 1,200 mg/day and phenytoin 250 mg/day to control occasional adversive seizures. A coagulation study following infusion of 5,000 units of AT III was carried out. Warfarin was discontinued the day before the study. 0.64 U/kg of AT III administration resulted in a 1% increase in AT III level after the infusion. The biological half life of AT III was 14.4 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral venous thrombosis with familial antithrombin III deficiency]. 404 Dec 90

There have been numerous accounts of women on ovulation inhibitors developing hypertension or reactifying or intensifying previous hypertension. Concerning frequency of significant hypertension in pill users, there are reports varying from .66% (or even 0%) to 19%. The time interval between start of medication and manifestation of hypertension also varies according to different sources from 7 days to 5 years, with the critical point usually around 6-8 weeks. Degree of hypertension after ovulation inhibitors ranges from mildly significant increases in systolic and/or diastolic blood pressure to malignant hypertension with irreversible kidney insufficiency. Early observable symptoms of hypertension include migrainelike headaches and rapid weight gain (sodium and water retention). After discontinuation of the medication, normal blood pressure is attained either within a few days or after 6-8 months. If normalization of blood pressure does not occur spontaneously there may be other causes (e.g., secondary vascular disorders). Concerning pathogenesis of ovulation-inhibitor-related hypertension, changes (increases) in the renin-angiotensin-aldosterone system are assumed to play a major role (almost all women on the pill exhibit elevated renin-angiotensin-aldosterone activity). Sodium retention may also be determinative. Many clinical and laboratory studies have demonstrated that it is the estrogen content of ovulation inhibitors that is responsible for the increased plasma renin activity. The study recommends: 1) women who wish oral contraceptive therapy should give careful family and personal histories and be tested for blood pressure before and during treatment (monthly, then after 6 months twice yearly); 2) careful supervision is indicated for women with high blood pressure or other cardiovascular disorders in their history, present or former kidney disorders, arterial hypertension, pregnancy toxemias, adipositas, or diabetes mellitus; 3) abnormal weight gain may be an early symptom; 4) if any rise in blood pressure is observed, ovulation inhibitor medication should be discontinued immediately; and 5) ovulation inhibitor-induced hypertension should be considered in differential diagnosis in young women with arterial hypertension.
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PMID:[Oral contraceptives and arterial hypertension]. 437 45

Effects of a new low-dosage combination oral contraceptive containing .5 mg WY3707 (a progestational substance) plus .05 mg ethinyl estradiol were studied on 30 normal women. Findings based on 25 patients remaining in the study for 5 months indicate a weight gain (64%), a tendency to hypo- and oligomenorrhea (58.3%), headache (52%), dizziness (44%) and nausea (20%) as common side-effects. Blood pressure recordings were below 140/90 and had no major variations. Blood sodium and potassium levels, measured before therapy initiation and 2 and 5 months after use, showed no significant changes. Discussion centers on 20 previous studies relating oral contraceptives to blood electrolytes and pressure and weight and menstrual changes.
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PMID:Effect of a new low-dosage oral contraceptive pill on blood electrolytes. A combined clinical and laboratory evaluation. 576 88

Fifty-one patients with essential hypertension, 22 males and 29 females with a mean age of 51 (range, 28 to 65 years), were studied for more than 12 months in a controlled clinical trial with nitrendipine, a new calcium antagonist agent. No differences in age, severity of hypertension, and other risk factors between the two sexes were detected. Forty-four of 51 patients completed the study, and 38 (86.4%) achieved a normalization of blood pressure. Mean systolic blood pressure decreased from 196.0 +/- 12.9 mm Hg (means +/- SD) during placebo to 171.2 +/- 9.5 mm Hg (12.6%, p less than 0.001) after 12 months. Mean diastolic blood pressure at the same time decreased from 109.0 +/- 5.2 mm Hg to 88.5 +/- 3.6 mm Hg (18.8%, p less than 0.001). Heart rate also decreased slightly but significantly (p less than 0.01) after the fifth week. A significant change in weight was not observed throughout the trial. Plasma potassium remained unchanged during the year, and plasma sodium after a transient increase (p less than 0.001) in the fifth week returned very close to basal levels in the sixth month. Side-effects were observed in 17 patients, 5 of whom had to leave the trial, but in the rest they were usually mild and transient. These were mainly frontal and occipital headache, facial flushing, ankle and pretibial oedema, and dizziness. No relationship was detected between side-effects and body weight or plasma sodium disturbances. Preliminary data on a separate group of 27 elderly patients (66-83 years) showed a better and faster effect of nitrendipine given in low doses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience with long-term nitrendipine treatment in essential hypertension. 608 73

The syndrome of tumor-induced osteomalacia has been previously thought to occur only in association with mesenchymal tumors, although one report has linked prostatic carcinoma with the syndrome. We report the case of a patient who presented first with the clinical and biochemical features of the syndrome of inappropriate antidiuretic hormone secretion, and then oncogenic osteomalacia. The first syndrome was characterized by headaches, nausea, and vomiting; serum sodium determinations ranged between 107 and 118 meq/L with simultaneous urine spot sodium concentrations of 100 to 116 meq/L. The circulating antidiuretic hormone level was markedly elevated to 261.5 microU/mL. The osteomalacia was discovered incidentally when depressed serum phosphorus levels of 1.2 to 1.7 mg/dL were noted in association with 24-hour urine phosphorus excretion exceeding 1000 mg/24 h. Undecalcified tetracycline-labeled bone biopsy samples confirmed oncogenic osteomalacia. Only afterward was a small-cell carcinoma of the lung identified as the likely source of both of these syndromes.
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PMID:Oncogenic osteomalacia and inappropriate antidiuretic hormone secretion due to oat-cell carcinoma. 609 61

Six patients with Nelson's syndrome were given sodium valproate with or without diazepam for 3 or 5 weeks. Initial high plasma adrenocorticotropic hormone (ACTH) concentrations were greatly reduced by treatment and returned to high levels when treatment was stopped. Diazepam did not add significantly to the effects of sodium valproate alone. Three patients reported a decrease in the severity and frequency of headaches while on sodium valproate. In five patients abnormal skin pigmentation was reduced. Sodium valproate is a gamma-aminobutyric acid (GABA) transaminase inhibitor and it is suggested that the drug raises GABA levels in the hypothalamus and that this is responsible for the reduction in ACTH secretion. The data are consistent with the hypothesis that Nelson's syndrome is a neuroendocrine disease caused by a deficiency in the hypothalamic GABA-ergic system.
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PMID:Effect of treatment with sodium valproate and diazepam on plasma corticotropin in Nelson's syndrome. 611 28


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