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)

An awakening has taken place over the last 25 years to the science of sleep disorders. Foremost amongst these, both in the medical world and the public eye, has been Sleep Apnoea Syndrome (SAS). The prevalence is thought to be the order of 1-2%. Males are eight times more commonly affected than females, although after the menopause the gap narrows considerably. Sleep apnoea occurs in children, usually in relation to large tonsils and adenoids, but in adult life patients usually present between the age of 40 and 60 and the prevalence increases with age. Numerous apnoeas or hypopnoeas during the night's sleep result in disordered sleep architecture and unrefreshing sleep. This is usually accompanied by night-long snoring which may lead to marital discord and even complaints from neighbours. Symptoms on waking may be a headache and a feeling of not being refreshed by sleep. Sleepiness during the day can interfere with work and social activities and may produce risks to the patient and others if it occurs while operating dangerous machinery or driving. Over a longer time scale SAS results in intellectual and memory deterioration, a higher incidence of ischaemic heart disease, hypertension, polycythemia and pulmonary hypertension. Right heart failure is particularly likely if there is chronic airflow obstruction contributing to a low arterial oxygen level. Asystolic periods and tachyarrhythmias may occur during apnoeic periods. The increased mortality of SAS relates to coronary and cerebrovascular disease and arrhythmias. Sudden death occurs with greater frequency in patients with SAS, mainly at night.
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PMID:Sleep apnoea: causes, consequences and treatment. 141 52

Sleep-disordered breathing may occur in a wide variety of neuromuscular syndromes, and may present with diverse, often isolated, symptoms or findings such as excessive daytime sleepiness, pulmonary hypertension, congestive heart failure, morning headaches, or hypoxia-induced nocturnal seizures. The authors report two sisters with congenital muscular dystrophy in whom central sleep apnoea resulted in the isolated symptom of nocturnal seizures in one, and morning headaches in the other. Review of the literature reveals that sleep-disordered breathing may be common in neuromuscular disorders, and may often be present when clinical weakness is mild, and insufficient to result in diurnal respiratory dysfunction.
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PMID:Central sleep apnoea in congenital muscular dystrophy. 194 Sep 43

Clinical experience with long-term nifedipine treatment in 23 patients aged between 1 1/12 and 14 8/12 years is reported. The cardiopulmonary diseases comprised primary pulmonary diseases with pulmonary hypertension (n = 4), congenital heart defects with intracardiac shunts and pulmonary hypertension which either were inoperable as a result of an Eisenmenger reaction (n = 7) or presented a high surgical risk (n = 5), or defects in which pulmonary hypertension did not regress despite corrective (n = 1) or palliative surgery (n = 3), and congenital defects without pulmonary hypertension (n = 3). Subjective improvement with an increase in physical performance was clearly observed in 15 cases. Echocardiography and cardiac catheter examinations showed no progression of the pulmonary arterial diseases, except in 1 patient with severe primary pulmonary hypertension and an 11-year observation period with nifedipine treatment during the last 4 years. No complications occurred during the 4 corrective operations. A patient aged 14 8/12 years with the Down syndrome and atrioventricular septal defect developed easily controllable heart failure during 7-day administration of nifedipine without additional cardiotherapy. 4 children initially suffered from flushed face and scalp, in one case with headache; 2 children reported fatigue. Long-term treatment with nifedipine should begin with strict 7-day supervision in hospital and possibly additional digitalization. Success of the treatment was determined by an improved quality of life in patients with primary pulmonary hypertension and inoperable defects, and by a reduced perioperative risk and postoperative regression of pulmonary hypertension in patients with operable defects.
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PMID:Experience with long-term nifedipine therapy in paediatric cardiological patients. 211 16

A clinical syndrome identical to the chronic mountain sickness of the Andes occurs commonly in Lhasa, Tibet. It affects, almost exclusively, the immigrant Han population and develops after an average of 15 years' residence at high altitude. The early symptoms are attributable to polycythaemia--headache, dizziness, loss of memory and fatigue being prominent. In the later stages of the disease, dyspnoea and peripheral oedema develop. Haemodynamic investigations show pulmonary hypertension with a normal cardiac output and dilatation of the right ventricle in the long-established case. Respiratory gas studies provide evidence of alveolar underventilation and ventilation: perfusion inhomogeneity. Both clinical and investigatory data suggest that the earlier stages of the disease are dominated by polycythaemia, while cardiopulmonary involvement increases with the duration of the disease. The disease is rare in women and uncommon in Tibetans. Cigarette smoking appears to be a contributory factor.
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PMID:Chronic mountain sickness in Tibet. 251 94

Urapidil is a postsynaptic alpha 1-adrenoceptor antagonist with a pharmacodynamic profile similar to prazosin. Unlike prazosin, however, urapidil also has some central activity which may explain the apparent improved tolerability of urapidil, including the absence of first-dose syncope. In clinical trials urapidil therapy resulted in significant reductions in blood pressure in patients with mild to severe essential hypertension, with little influence on heart rate. It is an effective antihypertensive when administered as monotherapy or in combination with beta-blockers and thiazide diuretics. In the few patients with cardiac dysfunction who have been studied to date, urapidil has improved myocardial oxygen consumption, systemic vascular resistance, left ventricular function, cardiac output and pulmonary capillary wedge pressure; however, further study is needed to assess the full therapeutic potential of urapidil in these patients. Urapidil has also been used successfully in the treatment of hypertensive emergencies, including eclampsia and pre-eclampsia, hypertensive crisis and hypertension occurring during general and cardiac surgery, rapidly lowering blood pressure without altering heart rate. Urapidil does not affect lipid or glucose metabolism, nor does it impair renal function. In addition, urapidil may be beneficial to patients with pulmonary hypertension, in whom it dilates pulmonary vascular beds to a greater extent than systemic vasculature, although therapeutic trials have not examined this effect. The most common adverse effects associated with urapidil therapy are dizziness, nausea, headache, fatigue and palpitations; however, these tend to be mild and transient and usually do not require discontinuation of treatment. Thus, urapidil offers a useful alternative to currently available drugs for the treatment of mild to severe hypertension, either as monotherapy or in combination with other antihypertensive drugs.
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PMID:Urapidil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the treatment of hypertension. 269 46

Profound transient nocturnal hypoxemia is common during REM sleep in "blue bloaters" with chronic obstructive lung disease, these patients having hypoxemia and CO2 retention when awake, when breathing air. These hypoxemic episodes appear to be due to a combination of reduced ventilation in REM sleep with a possible increase in the maldistribution of ventilation to perfusion within the alveoli at that time, and a reduction in functional residual capacity. The episodes are associated with exacerbations of pulmonary vasoconstriction, which can be reversed by oxygen therapy throughout sleep. Cardiac arrhythmias and alterations in ST segments are also found in these patients during sleep when breathing air. It is probable that the severity of hypoxemia in REM sleep can be predicted from knowledge of the arterial PO2 when breathing air when awake in patients with COPD. If so, expensive sleep studies are not essential to indicate the presence of hypoxemia in sleep in these patients, but such studies may be required in obese patients, in those who snore, or those who complain of headache following nocturnal oxygen therapy to demonstrate the presence of the overlap syndrome, in which obstructive sleep apnea is combined with chronic obstructive lung disease in the same patient. Nocturnal oxygen therapy may be dangerous in such patients with the overlap syndrome but appears to cause little rise in PCO2, in patients with COPD and REM-associated hypoxemia alone. Hypoxemia and sleep quality can probably be improved by oxygen therapy in "blue bloaters," and this treatment can also reverse pulmonary hypertension in REM sleep. The new ventilatory stimulant almitrine can also correct hypoxemia, without disturbing sleep quality, but the effects of this drug on pulmonary vasoconstriction during REM sleep are as yet unknown.
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PMID:Sleep in chronic obstructive lung disease. 293 59

The authors present some literature and their own data on the antiphospholipid syndrome (venous and arterial thromboses; obstetric pathology: spontaneous abortions and intrauterine death of a fetus; CNS involvement: from headaches and disorientation to psychic disorders and cerebral infarctions; thrombocytopenia, early aseptic osteonecrosis and pulmonary hypertension). Altogether 58 patients with lupus erythematosus and 20 patients with a complicated obstetric history were examined. Lupoid anticoagulant and antibodies to cardiolipin were revealed in 27 patients. The determination of antiphospholipid antibodies was shown to be of practical value from the view-point of the knowledge of humoral immunity disorders in systemic lupus erythematosus, more detailed clinico-laboratory characterization of patients, the diagnosis and prediction of disorders of the blood coagulation system, and the development of obstetric pathology.
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PMID:[Clinical value of determining the levels of lupus anticoagulant and anti-cardiolipin antibodies]. 314 84

Fourteen patients, 2 to 20 years old were investigated. Two had primary pulmonary hypertension, 11 had congenital heart disease and post-tricuspid shunts, and 1, a 20-year-old patient, was investigated after he had undergone surgical correction of truncus arteriosus I. Pulmonary arterial pressure, pulmonary flow index, peripheral systolic blood pressure and heart rate were measured before, and several times after intrapulmonary injection into the pulmonary artery of 0.5 microgram nifedipine/kg. Six patients were given an additional dose of 1 microgram nifedipine per kilogram into the pulmonary artery and hemodynamic measurements were repeated. In eight children, receiving 100% oxygen via a breathing mask, nifedipine effects were compared with oxygen effects. After 10 minutes under oxygen, the same hemodynamics were determined as after nifedipine. In addition, in four of these children aortic pressure and arterial oxygen saturation were also measured. Maximal effects occurred within 4 minutes. 0.5 micrograms nifedipine per kilogram caused a slight reduction in mean pulmonary arterial pressure (p less than 0.05), as well as increase in pulmonary flow index (p less than 0.005). However, no significant change in heart rate or in systolic blood pressure was observed. 1 microgram nifedipine per kilogram IP had almost the same effects. No adverse side effects occurred, besides mild headaches in one child. A comparison of nifedipine injected into the pulmonary artery with oxygen breathing in congenital heart disease combined with pulmonary hypertension, is reported for the first time. Nifedipine had a more pronounced and beneficial effect with a selective action on the pulmonary vascular bed.
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PMID:Hemodynamic effects of nifedipine and oxygen in children with pulmonary hypertension. 315 41

Sleep apnoea syndromes are a frequent disease, with an incidence of more than 1% in the adult population, a strong male predominance, and a maximal frequency between 40 and 60 years. Their clinical manifestations are dominated by snoring and daytime sleepiness, at times associated with morning headaches, intellectual deficiency, sexual impotence. Obesity, hypertension and polycythemia are not uncommon. These patients are at risk for accidents due to sleepiness, sudden death due to sleep apnoea-related cardiac arrhythmias, ischemic attacks related to hypertension and polycythemia and right heart failure secondary to pulmonary hypertension and alveolar hypoventilation. The most frequent form of sleep apnoea syndromes include obstructive and mixed apnoeas. Their mechanism involves both anatomic factors (upper airway narrowing) and functional factors (defective activation of upper airways dilatory muscles) which lead to upper airway occlusion upon inspiration during sleep. Two therapeutic strategies are possible: a surgical one, uvulopalatopharyngoplasty, the efficacy of which is inconstant and unpredictable and nasal continuous positive airway pressure, which is constantly efficacious but constraining. Central sleep apnoea syndromes are rare, less clearly defined and more difficult to treat.
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PMID:[Sleep apnea syndromes in adults]. 332 Dec 51

This review was limited to topics of current concern with respect to the use of oral contraceptives (OCs). Thromboembolism, liver injury, fertility and infertility, miscellaneous adverse effects (such as headaches and psychological and metabolic effects), and acceptance were the topics covered. It was found that the risk of death due to pulmonary embolism or cerebral thrombosis among users of OCs amounted to 1.5 per 100,000 women aged 20-34 years as against .2 for a comparable group not using drugs; for users 35-44 years old the risk rose to 3.9 per 100,000 compared to .5 for nonusers. The increased risk associated with suppression of lactation by administration of diethylstilbestrol was most striking among women over 25 years of age; in this group the risk was 10-fold greater than that of lactating mothers. 1 report suggested that women with pulmonary hypertension due to congenital heart disease should probably not receive OCs. Contraindications to the use of OCs must now include any history of thromboembolic disease or disorders of the blood-clotting mechanism. There appeared to be a predisposing factor among women who develop jaundice while taking OCs. A remarkable number of such subjects had had idiopathic jaundice of pregnancy. There seems to be little evidence for permanent liver damage but very definite evidence for bile stasis and transient morphological changes. Much more work needs to be done before any adverse effect on fertility is established. In cases where fertility reduction is suspected, it must be demonstrable that fertility prior to the use of OCs was unimpared. Among 20 patients on OCs who had had migraine, the attacks became more intense and their frequency increased for 15 of the 20 patients. Generally speaking, those using the intrauterine device (IUD) were more persistent in accepting the method than those on OCs probably because the IUD may be used more extensively than OCs in underdeveloped countries.
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PMID:Effects of oral contraceptives. 489 31


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