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

10 cases are presented in which a posterior cerebral artery (PCA) deficit developed suddenly in dramatic fashion with headache, visual symptoms, sensory and motor deficits, and signs of 3rd nerve involvement. There were 9 females and 1 male, ranging in age from 18-51 years with 7 cases under age 35. In 9 of the 10 patients, headache was prominent at the onset; 6 patients reported being dramatically stricken with a severe, sharp localized pain in the forehead or occiput. Visual symptoms were prominent at the onset in 7 patients -- 4 patients experiencing blindness and 3 patients a hemianoptic deficit. Hemisensory symptoms or deficit occurred in 6 instances, a hemiparesis in 3, combined weakness and sensory deficit in 1. Evidence of a 3rd nerve palsy was found in 3 cases. A persisting neurologic deficit occurred in 10 cases -- visual field defect, 6 cases; hemiplegia, 1; slight weakness, 1; and a sensory deficit, 2. A movement disorder developed on the involved side in 7 cases. Evidence of infarction in 1 or both occipital lobes was obtained in 6 patients. 1 patient did not have impaired visual fields, and the other 3 were examined before the days of nuclear medicine and CT scanning. Conventional angiography was performed in 8 patients with the following results: retrothalamic occlusion of 1 PCA (1 patient); distal occlusion of 1 PCA (1 patient); retrothalamic narrowing of 1 PCA (1 patient); irregularity of the wall of the upper basilar artery and both PCAs (1 patient); and in 4 angiography was normal. A digital subtraction angiogram in 1 patient was normal; 1 patient did not have an arteriogram. A history of accompanied migraine was obtained in 3 patients. 1 patient was pregnant; 1 patient was 3 months postpartum. 1 patient was taking oral contraceptives; 1 patient had taken 1 contraceptive pill, and 1 patient was receiving injections of estrogen. These cases represent involvement of the territory of the PCA. They share the same features in varied combinations. The onset or evolution is dramatic, distinctive, or alarming. The cases do not fall easily into any commonly recognized category of cerebrovascular disturbances. The process that most likely applies to this group of cases is migraine. If that is so, the term "catastropic migraine" or "cataclysmic migraine" may have some currency. If it is assumed that the process is ischemic and since vascular obstruction was found in 2 cases, the possibility of using heparin therapy might be considered. In most of the present cases, steroid therapy was used to control brain swelling. If the pathologic process is temporary vasospasm, the use of hemodilution or hyperbaric oxygen could be an option.
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PMID:Unusual vascular events in the territory of the posterior cerebral artery. 395 50

From January 1980 to August 1983, 213 patients with carbon monoxide poisoning were seen; 131 received hyperbaric oxygen and had no sequelae. Eighty-two patients were treated with normobaric oxygen; ten (12.1%) returned with clinically significant sequelae. The specific neurological sequelae included headaches, irritability, personality changes, confusion, and loss of memory. This recurrent symptomatology developed within one to 21 days (mean, 5.7 days) after the initial exposure, although no reexposure occurred. These recurring symptoms resolved rapidly with hyperbaric oxygen therapy. We recommend that hyperbaric oxygen therapy be used whenever CO poisoning symptoms recur.
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PMID:Subacute sequelae of carbon monoxide poisoning. 406 87

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
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PMID:[Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage]. 409 85

A total of 100 outpatients in the North-East of Scotland were given a simple anaesthetic of propanidid, nitrous oxide, oxygen, and halothane. The study was undertaken to assess what happened to patients when they left hospital after outpatient surgery. An outpatient questionnaire was used, and results show that 31% of patients journeyed home unaccompanied by a responsible person, 73% of car owners drove within 24 hours of the operation, and 9% drove themselves home. Postoperative symptoms of drowsiness (26%), headache (27%), nausea (22%), and dizziness (11%) were recorded, and a higher incidence of symptoms was recorded when surgery exceeded 15 minutes. A new form for outpatient operative procedures in Aberdeen has been devised with modern legal implications in mind.
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PMID:An assessment of postoperative outpatient cases. 464 94

The effect of vasodilation (with nifedipine) or beta-adrenergic receptor blockade (with propranolol, alprenolol or metoprolol) on the rate of rise of oxygen uptake and heart rate were studied in 14 healthy subjects after a step-wise increase of workload from a light to a moderate exercise intensity. Under beta-adrenergic receptor blockade steady state oxygen uptake at both workload levels was equal to control values; heart rate went up to 111 min-1 (s.d.:15) vs 150 min-1 (s.d.:24) for the control experiments. The half-times of the oxygen uptake transient were unchanged. After vasodilation with nifedipine heart rates were higher (20% for the lower and 12% for the higher exercise level) but steady state oxygen uptake levels and rate of rise were also unchanged. It is concluded that the rate of rise of oxygen supply to working skeletal muscles after a stepwise increase of load is not reduced either by a beta-adrenergic receptor blocking drug nor by a vasodilating agent. Discomfort during exercise appears to be a subjective phenomenon related to reduced skin circulation and sweating under beta-adrenergic receptor blockade, or to headache and congestion after vasodilatory drug administration. These side-effects are not caused by a reduced oxygen supply of muscle, neither under steady state situations nor under rapid changing workload conditions.
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PMID:Transient in oxygen uptake after step-increase of workload under beta-adrenoceptor blockade or vasodilation. 613 56

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

Iloprost is a chemically stable derivative of carbaprostacyclin. We studied its hemodynamic effects in 10 patients in an intensive care unit. Iloprost was infused intravenously for 3 days for the treatment of advanced obliterative arterial disease of the lower extremities. Clinically significant hemodynamic responses were obtained with an infusion rate of 0.5 ng/kg/min. All subjects tolerated the dose of 4 ng/kg/min, which increased heart rate an average of 11% and cardiac index an average of 26%. This infusion rate decreased mean arterial pressure by 15%, total peripheral resistance by 31%, and pulmonary vascular resistance by 34%. Mean pulmonary arterial pressure, pulmonary capillary wedge pressure, left and right ventricular stroke work indices, and rate pressure product did not change. At higher doses of up to 8 ng/kg/min, responses were augmented only slightly, but side effects such as headache, nausea, and abdominal colics became more prominent. The data show iloprost to be a potent vasodilator that reduces both pre- and afterload and presumably induces a compensatory increase in cardiac output and heart rate, but does not increase the work load or oxygen demand of the heart.
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PMID:Hemodynamic effects of iloprost, a prostacyclin analog. 620 78

Antihypertensive vasodilators share the capability of producing vasodilation of arterioles. In addition, two of them, i.e. nitroprussiate and prazosine, also produce vasodilation of veinulae. Both of these agents cause a simultaneous decrease in pre-load and post-load, and may be used in heart failure. The effectiveness of vasodilators is offset by regulatory cardiac and/or renal mechanisms, and the association with a sympatholytic agent and/or a diuretic is generally needed. Consequently, vasodilators are usually the third step in the course of managing a hypertensive patient. Association with a betablocking agent is especially necessary in patients with coronary insufficiency, in order to prevent an increase in myocardial oxygen requirements and worsening of angina pectoris. Vasodilators are active within a fairly wide dosage range, making individualized dosages requisite. In treating hypertension by the oral route, daily doses above 200 mg for dihydralazine, 60 mg for minoxidil and 10 mg for prazosine are only exceptionnaly useful. In emergency treatment of hypertension, diazoxide and nitroprussiate can be used only in patients under continuous cardiovascular monitoring. Nitroprussiate must, in addition, be given through a controlled infusion device, but ensures more flexible and safer control of blood pressure. Dihydralazine may produce headache. This side effect occurs very early and is hardly compatible with continuation of treatment. Long term side effects are very uncommon or strictly biological for dosages below 200 mg/day. With currently used dosages (20 to 60 mg per day) minoxidil consistently produces hypertrichosis, outruling its protacted use in women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antihypertensive vasodilators]. 631 28

The recently introduced preparation of intravenous glyceryl trinitrate (nitroglycerin) provides a rapid steady therapeutic blood concentration of nitrates during continuous infusion. Intravenous glyceryl trinitrate causes venodilation at low doses, but at higher doses dilates both arteries and veins. Its principal haemodynamic effects at therapeutic dosages include a decrease in blood pressure in preload (left ventricular filling pressure) and in determinants of afterload, and a decrease in myocardial oxygen demand. Human pharmacokinetic data are few and difficult to interpret due to wide interstudy and interindividual variation. There is no close correlation between infusion rate, blood concentration and haemodynamic effects. The nature of the patient population treated with intravenous glyceryl trinitrate has largely precluded the use of a placebo, but in open trials the drug has been used successfully in the treatment of unstable angina, left ventricular failure accompanying acute myocardial infarction and in the control of hypertension associated with cardiac surgery at dosages titrated to achieve a specific end-point. Favourable haemodynamic responses have been achieved in very short term studies in congestive heart failure, and preliminary studies suggest that institution of intravenous glyceryl trinitrate early after acute myocardial infarction may limit ischaemic damage. However, use of the drug in acute myocardial infarction remains controversial. Intravenous glyceryl trinitrate is generally well tolerated, although hypotension and headache occur occasionally, and sinus tachycardia and bradycardia less frequently. Careful titration of dosage is required (beginning at 5 micrograms/min), and if the infusion sets contain polyvinylchloride, the delivered dose is lower than that calculated, because of adsorption of glyceryl trinitrate onto the plastic tubing.
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PMID:Intravenous glyceryl trinitrate (nitroglycerin). A review of its pharmacological properties and therapeutic efficacy. 642 Jan 39

We studied the effect of supplemental nocturnal oxygen on blood gases in 15 patients with severe but stable chronic obstructive lung disease (ratio of forced expired volume in one second to forced vital capacity, 37.2 +/- 1.8 [mean +/- S.E.] per cent of predicted; arterial oxygen tension, 50.7 +/- 1.4 mm Hg; and arterial carbon dioxide tension [PCO2], 53.1 +/- 1.5 mm Hg). Sleep variables and measures of gas exchange were determined on two consecutive nights; on the first night the subjects breathed supplemental oxygen, and on the second they breathed room air. Transcutaneous PCO2 was measured with an infrared sensor, and arterial oxygen saturation with an ear oximeter. Breathing of supplemental oxygen sufficient to keep oxygen saturation at or above 90 per cent was associated with only small increases (less than 6 mm Hg) in PCO2 throughout sleep, as compared with values while subjects were breathing room air. The increase in PCO2 occurred early in the night and was not progressive. Only three patients, who were found to have obstructive sleep apnea in addition to obstructive lung disease, had larger increases in PCO2 during sleep and reported morning headaches. We conclude that nocturnal oxygen does not induce clinically important increases in PCO2 during sleep in patients with stable obstructive lung disease and therefore can safely be used to prevent the dangerous consequences of hypoxia.
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PMID:Effect of supplemental nocturnal oxygen on gas exchange in patients with severe obstructive lung disease. 642 Jul


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