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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

In 1983, a previously healthy 21-year old mother came to University Hospital in Dijon, France feeling weak and had a severe frontal headache with vomiting. Clinical and biochemical tests were normal. She smoked 20 cigarettes/day and used a high dosed combined oral contraceptive (OC) (ethinyl estradiol and cyproterone acetate). 15 days later, the headache returned and she could not understand spoken words and the bilateral section of the brain had slowed. Yet her mental status was normal as were cerebrospinal fluid and cerebral computerized tomography tests. The antiherpes virus drug, vidabarine, did not alleviate symptoms. At least 1 month later, a severe left pulmonary embolism caused acute right heart failure. She also had a prethrombotic left iliac vein, so physicians began heparin therapy, adding nifedipine and buflomedil to control the spasms in the right internal iliac artery and both external iliac arteries. Acute ischemia of the lower limbs eased within a week but sensory disorders remained for 2 months. Satisfactory collaterality transpired due to a blocked left external iliac artery and left iliac vein. The following signs and symptoms indicated her condition to be homocystinuria: blond hair with deep blue eyes, macrocytic anemia, factor VII deficit (51%), strong positive Brandt's reaction, cystine homocystine in the plasma, and presence of homocystine, cystathionine, and methionine in the urine. Physicians took her off the OC and discharged her on vitamin B6/day, folic acid/day, betaine citrate/day, and the anticoagulant Coumadin. A subsequent check of her 19-year old sister found she had it too. They assessed the patient's condition yearly. In 1988, her left leg developed edema and she limped when not using elastic stockings. Effects of iliac vein phlebitis were evident. She no longer suffered from headaches. Since plasma methionine was within the normal range and homocystine no longer was present in plasma and urine, the physicians halted the anticoagulant therapy. In conclusion, the OC precipitated this partial form of homocystinuria.
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PMID:Vascular manifestations in homocystinuria. 161 Jun 63

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

Since 1981 the authors have performed 14 orthotopic heart transplantations and one heart-lung transplantation, using cyclosporine and prednisone as immunosuppressants. Eight of the recipients had terminal congestive cardiomyopathy and six had ischemic cardiac dysfunction. The combined heart-lung transplantation was performed on a patient with a congenital ventricular septal defect with Eisenmenger's syndrome. Twelve of the patients were alive and well at follow-up 9 to 34 months (mean 17.4 months) after transplantation. One patient died of acute rejection and one of acute pancreatitis and secondary peritonitis. The third death, due to acute right ventricular failure, occurred immediately after transplantation. Rejection was diagnosed histologically on seven other occasions in four patients and was treated successfully. Infection was not a major problem. Cyclosporine -induced reversible nephrotoxicity was evident in 12 patients, 2 of whom required dialysis. Other side effects of cyclosporine seen in these patients included hypertension, gastrointestinal upset, headaches and hirsutism. This experience suggests that cyclosporine is a potent immunosuppressive agent that has greatly reduced the hazards of rejection and infection. However, the frequency of nephrotoxicity is high; careful monitoring of cyclosporine blood levels and renal function is essential.
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PMID:Cyclosporine in cardiac transplantation. 623 93

Patients in hypercapnic respiratory failure have got a poor prognosis. The recognition of pathophysiological mechanisms is required in order to choose adequate therapy. During the past years it has been shown that pathological respiratory events during sleep occur early in the disease process and that blood gas changes are usually most pronounced during sleep. Minute ventilation and functional residual capacity (FRC) decrease during sleep even in normal subjects and upper airway resistance increases markedly. PO2 slightly decreases and paCO2 increases. In most patients with hypercapnic respiratory failure episodes of marked hypoxemia and hypercapnia occur, mainly during REM sleep. Suggested pathomechanisms are worsening ventilation-/perfusion mismatching, impaired respiratory muscle function and a reduction in ventilatory drive, the latter two being of major importance. The relation between load and capacity is shifted towards an increased load and ventilatory drive is decreased at the same time. Therapeutic strategies that reduce the load of the respiratory pump, increase minute ventilation and prevent sleep related hypoventilation, thus noninvasive ventilation should be used. Symptoms of hypercapnic respiratory failure are often unspecific. Dyspnea, headache and awakening from sleep with dyspnea are often reported. Signs of right heart failure will be present in advanced disease stages. Early diagnosis and treatment provided, noninvasive ventilation achieves excellent improvement of both quality of life and life expectancy, especially if the primary disease progress is not rapidly progressive.
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PMID:[Pathophysiology and clinical aspects of global respiratory insufficiency]. 923 56

A lack of respiratory centrogenic drive of undetermined origin is a rare cause of cyanosis. In this condition, voluntary hyperventilation restores arterial oxygen saturation to normal. Secondary changes consist of polycythemia, somnolence, headache and right heart failure. The present report of a 43-year-old thin man with idiopathic alveolar hypoventilation is combined with a review of 12 similar patients reported by others. His resting oxygen saturation increased from 60% to 98% with hyperventilation. The pulmonary artery pressure was 68/26 mm. Hg and cardiac output 12.3 l./min. Death resulted from pulmonary infarction, and no specific abnormalities were found in the brain.
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PMID:HYPOVENTILATION, CYANOSIS AND POLYCYTHEMIA IN A THIN MAN. 1409 5

Pulmonary arterial hypertension (PAH) is a rare debilitating disease characterized by an increase in pulmonary vascular resistance and progressive right ventricular failure. PAH may be primary or associated with other conditions such as collagen vascular disease, portal hypertension, and HIV. Intravenous epoprostenol improves the survival, exercise tolerance, hemodynamics, and quality of life in patients with PAH and is believed to work through multiple pathways including vasodilation, opposition of smooth-muscle hypertrophy, and inhibition of platelet aggregation. Common dose-limiting side effects are flushing, jaw pain, arthralgias, myalgias, and headache, which are attributed to the vasodilatory effects of epoprostenol. In clinical practice, patients often develop persistent rash that is distinct from the flushing associated with epoprostenol. The specific findings both on physical examination and on dermatopathology have not, however, been well described. This report describes the cutaneous and dermatopathologic findings of 12 patients who developed persistent rash while receiving long-term prostacyclin for PAH.
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PMID:Cutaneous findings in patients with pulmonary arterial hypertension receiving long-term epoprostenol therapy. 1524 33

Pulmonary arterial hypertension (PAH) is a rare disease characterized by vascular proliferation and remodeling, resulting in a progressive increase in pulmonary arterial resistance, right heart failure, and death. The pathogenesis of PAH is multifactorial, with endothelial cell dysfunction playing an integral role. This endothelial dysfunction is characterized by an overproduction of vasoconstrictors and proliferative factors, such as endothelin-1, and a reduction of vasodilators and antiproliferative factors, such prostacyclin and nitric oxide. Phosphodiesterase type 5 (PDE-5) is implicated in this process by inactivating cyclic guanosine monophosphate, the nitric oxide pathway second messenger. PDE-5 is abundantly expressed in lung tissue, and appears to be upregulated in PAH. Three oral PDE-5 inhibitors are available (sildenafil, tadalafil, and vardenafil) and are the recommended first-line treatment for erectile dysfunction. Experimental studies have shown the beneficial effects of PDE-5 inhibitors on pulmonary vascular remodeling and vasodilatation, justifying their investigation in PAH. Randomized clinical trials in monotherapy or combination therapy have been conducted in PAH with sildenafil and tadalafil, which are therefore currently the approved PDE-5 inhibitors in PAH treatment. Sildenafil and tadalafil significantly improve clinical status, exercise capacity, and hemodynamics of PAH patients. Combination therapy of PDE-5 inhibitors with prostacyclin analogs and endothelin receptor antagonists may be helpful in the management of PAH although further studies are needed in this area. The third PDE-5 inhibitor, vardenafil, is currently being investigated in PAH. Side effects are usually mild and transient and include headache, flushing, nasal congestion, digestive disorders, and myalgia. Mild and moderate renal or hepatic failure does not significantly affect the metabolism of PDE-5 inhibitors, whereas coadministration of bosentan decreases sildenafil and tadalafil plasma levels. Due to their clinical effectiveness, tolerance profile, and their oral administration, sildenafil and tadalafil are two of the recommended first-line therapies for PAH patients in World Health Organization functional classes II or III.
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PMID:Phosphodiesterase type 5 inhibitors in pulmonary arterial hypertension. 1976 39

Pulmonary arterial hypertension (PAH) is a progressive and fatal disease characterized by increasing pulmonary vascular resistance leading to right ventricular failure and death. Treprostinil is a stable prostacyclin analog approved for the treatment of PAH to improve exercise capacity. In the setting of PAH, the major pharmacological actions of treprostinil include vasodilatation of the pulmonary and systemic vascular beds, inhibition of platelet aggregation and inhibition of smooth muscle cell proliferation. Treprostinil therapy may be delivered via parenteral (subcutaneous and intravenous) or inhaled routes of administration, with oral tablets in the later stages of clinical development. In clinical trials, treprostinil has been shown to improve clinical status, functional class, exercise capacity and quality of life. Common side effects of treprostinil therapy include headache, flushing, jaw pain, diarrhea, and for subcutaneous administration, infusion site pain or reaction. This article provides an overview of treprostinil therapy for the treatment of PAH with a focus on the available efficacy and safety data for parenteral, inhaled and oral administration.
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PMID:Treprostinil for the treatment of pulmonary arterial hypertension. 2325 41

Right atrial myxomas are rare primary tumors of the heart. They may remain asymptomatic or eventually cause constitutional signs and symptoms. Less frequently, obstruction of the tricuspid valve occurs, resulting in exertional dyspnea, syncope, or sudden death. Neurological manifestation as initial presentation of atrial myxomas is rarely, if ever, associated with right atrial myxomas and may be secondary to cerebral infarction, cerebral hemorrhage and, more rarely subarachnoid hemorrhage. We review the case of a previously unknown, middle-aged Nigerian man who presented to hospital with severe headache and sudden loss of consciousness. A clinical diagnosis of hypertensive hemorrhagic cerebrovascular accident was made. The patient died suddenly a few hours after presentation. Post-mortem examination revealed a small intracerebral hemorrhage in the left superior temporal lobe as well as a large right atrial myxoma, a ventricular septal defect in the muscular septum, and right ventricular hypertrophy. The liver showed fatty change while the kidneys showed evidence of benign nephrosclerosis. Right atrial myxomas may, therefore, be remotely considered as a cause of intracranial hemorrhage, especially in the presence of predisposing cardiac anomalies such as a ventricular septal defect. Similarly, being a known cause of right heart failure, sudden death, and other constitutional derangements, it may contribute significantly to disease outcome. Hence, it should be given due consideration in the differential diagnosis of cerebrovascular accidents.
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PMID:Right atrial myxoma as a possible cause of hemorrhagic stroke and sudden death. 2327 55


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