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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

Six patients with episodic cluster headache were investigated as to blood pressure, heart rate, cerebrospinal fluid pressure (Pcsf) and frontal vein pressure (Pvf) during five nitroglycerin (NG) provoked attacks and one spontaneous attack. In a seventh studied patient the NG failed to provoke an attack. The earlier reported decrease of systolic blood pressure and increase of diastolic blood pressure and heart rate after NG administration were also found in these patients. The "dynamite headache" was related to the start and duration of an increase of the cerebrospinal fluid pressure. There was no relationship between the start or the maximum pain of the cluster headache attack and changes in Pcsf or Pvf. On breathing oxygen during a cluster headache attack, there was a decrease of Pcsf but in some patients a temporary increase of Pvf was observed, which possibly indicates that oxygen simultaneously attains constriction of arteries and veins.
Headache 1992 Oct
PMID:Cerebrospinal fluid pressure and venous pressure in "dynamite headache" and cluster headache attacks. 144 86

Eighty-two patients were hospitalized following an accidental exposure to chlorine. All patients presented with dyspnoea and cough. The other symptoms included irritation of throat (53.6%), irritation of eyes (42.3%), headache (29.2%), abdominal pain (26.8%), vomiting (24.3%) and giddiness (9.7%). All of them had bronchospasm and 5 (6%) had cyanosis at the onset. An x-ray of the chest revealed patchy infiltrates in 3 (3.85%) and hilar congestion in 2 (2.44%). Pulmonary function tests showed an obstructive pattern in 27.4%, restrictive in 3.25% and mixed in 53.2%. Pulmonary functions were normal in 16.1% of the patients. Bronchoscopy revealed tracheobronchial mucosal congestion in all cases, hemorrhagic spots in 35.7%, erosions and ulcers in 12.5%. All patients were treated with oxygen, aminophylline, hydrocortisone and antibiotics. Haematemesis (n = 1) and pulmonary oedema (n = 2) developed 12 hours after the admission. Two other patients developed pneumonia 48 hours later. All patients recovered satisfactorily. On follow-up 16 patients had no sequelae after one year. Pulmonary functions were normal in 5 patients after 3 years of follow-up.
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PMID:Acute accidental exposure to chlorine fumes--a study of 82 cases. 145 67

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.
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PMID:Acetazolamide and high altitude diseases. 148 96

Chronic mountain sickness, which affects permanent residents of high altitudes, is the outcome of a progressive loss of ventilatory rate which naturally occurs with age and resulting in excessive hypoxemia and polycythemia. A theoretical model predicts the progressive failure of homeostatic control of the hemoglobin concentration when the values increase above those found at sea level. This is confirmed by lack of feedback mechanism between high altitude erythrocytosis and serum erythropoietin. The results of epidemiological studies are in agreement with the physiological findings. In a male population living at 4,300 m, an increase with age of the prevalences of excessive erythrocytosis (Hb > 213 g/l), blood oxygen saturation < 83%, headaches and a high score of symptoms of chronic mountain sickness has been found. The studies suggest the possibility that in addition to an accentuated hypoxemia, the excessive erythrocytosis may also result from an overreaction of the bone marrow to a fixed level of hypoxemia in ageing individuals.
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PMID:Pathophysiology and epidemiology of chronic mountain sickness. 148 2

This study was designed to determine the relative speeds of induction and complication rates using either halothane or isoflurane for rapid inhalational induction of anaesthesia. Forty ASA physical status 1 and 2, unpremedicated patients presenting for day-care dental surgery received a rapid inhalational induction (RII) with either halothane 3.5% or isoflurane 5% in humidified oxygen. The carrier gas was humidified in order to limit airway irritation caused by the pungency of the volatile agents. Isoflurane produced a faster induction than halothane-121(50) (SD) sec vs 176(36) sec (P less than 0.01). Complication rates during induction (coughing, secretions, excessive movement and abandoned inductions) were similar for the two groups. The majority of patients in both the isoflurane group (17/20) and the halothane group (14/20) found the technique of RII to be acceptable. The incidences of headache, nausea and vomiting were low and not significantly different for the two groups. Isoflurane 5% in humidified oxygen is as acceptable for RII as halothane 3.5% and has a similar complication rate. Isoflurane may be used for RII in cases where it is deemed necessary to avoid halothane, or when a more rapid inhalational induction is required than is possible with halothane. The technique of RII with either agent in unpremedicated patients is well suited to day-care anesthesia.
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PMID:Rapid inhalational induction of anaesthesia with isoflurane or halothane in humidified oxygen. 155 Nov 55

We reviewed over 220 cases of acute carbon monoxide (CO) poisoning and now report on 17 patients whose poisoning occurred from the indoor use of propane-fueled forklifts. All patients in this series presented with neurologic symptoms or persistent headache and were given hyperbaric oxygen to resolve their symptomatology. We investigated the concentration of CO in the exhaust emissions of 12 propane-fueled forklifts used in various workplaces in our location. The average CO concentration in the exhaust during engine idling was 36,000 parts per million (3.6%). This value decreased slightly to 30,000 ppm (3.0%) at working engine speed. Measurements of exhaust flow indicate CO production rates of approximately 60 liters per minute at working engine speed. These quantities of CO constitute a significant occupational exposure risk to workers using propane-fueled forklifts in unventilated indoor environments.
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PMID:Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts. 144 89

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.
Headache 1992 Jan
PMID:Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction. 155 28

In this article we describe the clinical features, natural history, and clinical variants of cluster headaches, following the modern International Headache Society classification of cluster headaches in its two types: episodic and chronic. The basic pathophysiology is considered to be the trigeminal vascular system, the common final pain pathway, with pain initiated in a cyclical fashion by disordered central hypothalamic pacemaker. Oxygen, rapidly acting ergotamine, or dihydroergotamine preparations serve as abortive treatment of acute attacks; various pharmacotherapeutic options and combination therapies aid in the prophylaxis of cluster headache; and trigeminal radio frequency gangliorhizolysis is a very useful surgical approach in patients with chronic cluster headache who are resistant to medical treatment.
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PMID:Cluster headache. 817 May 85

Twenty-eight cluster headache patients were examined either in remission (n = 10), in the interparoxysmal period ("cluster phase") (n = 12), or during spontaneously occurring (n = 7), or nitroglycerin provoked (n = 7) attacks. Fourteen healthy controls participated in the study. Oxygen saturation (SaO2), end-tidal CO2 (PCO2), and respiratory rate (R.R.) were recorded for the controls and the patients during the different phases of cluster headache. Both PCO2 and SaO2 tended to be lower during the interparoxysmal period of the cluster phase when compared to the control group or to the remission. During both nitroglycerin-provoked and spontaneous attacks, PCO2 and SaO2 tended to respectively decrease and increase, both when compared with the "cluster phase" and with the period immediately prior to attack ("pre-attack"). Hence the "pre-attack" state may, on an average, be characterized by a slight hypoxia and a slight hyperventilation. Marked, clinically observable hyperventilation was present only in the occasional cluster headache patient. There was no SaO2 decrease from the "cluster phase" (interparoxysmal period) to the period immediately preceding the attack ("pre-attack"), and SaO2 "dips" preceding an attack were only observed in one cluster headache patient. As demonstrated previously by our group, a considerable lowering of SaO2 (i.e. partly to less than or equal to 83%) does only exceptionally lead to attack (Zhao et al, 1990). This observation combined with the evidence presented herein may seem to indicate that the slight pre-attack oxygen desaturation probably is too small to be a symptom-producing factor in cluster headache--be it in the spontaneously occurring or in the induced attack.(ABSTRACT TRUNCATED AT 250 WORDS)
Headache 1992 Mar
PMID:Cluster headache: oxygen saturation and end-tidal CO2 during and without attack. 156 43


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