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)

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.
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PMID:Analysis of neurologic symptoms in deep diving: implications for selection of divers. 232 22

The contrast agent Iotrolan 300 has potential advantages for bronchography over previous agents in that it can be injected directly through the bronchoscope and it does not obscure bronchoscopic vision or interfere with further bronchoscopic procedures. It was used for selective bronchography in 20 patients with suspected bronchiectasis. Side effects and change in FEV1 and in arterial oxygen saturation were compared in these patients and in 14 patients undergoing bronchoscopy for suspected carcinoma. Thirteen of the 20 patients undergoing bronchography had side effects, mainly headache, nausea, and a feeling of heat or flushing. The fall in FEV1 at four hours (0.3 l) did not differ from the fall in the control group (0.1 l). The fall in arterial oxygen saturation (SaO2) during bronchography (9.4%) did not differ significantly from the fall during bronchoscopy in the control group (6.1%). Iotrolan gave good quality bronchograms, which in all cases provided a diagnosis. Iotrolan appears to be suitable for bronchography by fibreoptic bronchoscope and to be well tolerated.
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PMID:Suitability of and tolerance to Iotrolan 300 in bronchography via the fibreoptic bronchoscope. 240 28

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."
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PMID:Myocardial ischemia induced by prostacyclin and iloprost. 240 9

Regional cerebral blood flow (rCBF) was measured in 16 cranial regions in 23 children and adolescents with frequent headaches using the non-invasive Xenon-133 inhalation technique. Blood flow response to 5% carbon dioxide (CO2) was also determined in 21 patients, while response to 50% oxygen was measured in the two patients with hemoglobinopathy. Included were 10 patients with a clinical diagnosis of migraine, 4 with musculoskeletal headaches, and 3 with features of both types. Also studied were 2 patients with primary thrombocythemia, 2 patients with hemoglobinopathy and headaches, 1 patient with polycythemia, and 1 with headaches following trauma. With two exceptions, rCBF determinations were done during an asymptomatic period. Baseline rCBF values tended to be higher in these young patients than in young adults done in our laboratory. Localized reduction in the expected blood flow surge after CO2 inhalation, most often noted posteriorly, was seen in 8 of the 13 vascular headaches, but in none of the musculoskeletal headache group. Both patients with primary thrombocythemia had normal baseline flow values and altered responsiveness to CO2 similar to that seen in migraineurs; thus, the frequently reported headache and transient neurologic signs with primary thrombocythemia are probably not due to microvascular obstruction as previously suggested. These data support the concept of pediatric migraine as a disorder of vasomotor function and also add to our knowledge of normal rCBF values in younger patients. Demonstration of altered vasomotor reactivity to CO2 could prove helpful in children whose headache is atypical.
Headache 1989 Jun
PMID:Regional cerebral blood flow in childhood headache. 250 64

Nitrates are old drugs, introduced into medical treatment more than 100 years ago, initially as a homeopathic remedy against headache (1850), and only later against angina pectoris (1867). Their typical hemodynamic, antiischemic effects were described in man in the 1950s and 1960s. They include: a reduction in venous return, lowering of the abnormally increased left ventricular enddiastolic pressure during ischemia, a decrease in left ventricular systolic wall stress, and changes in left ventricular geometry resulting in a decrease of myocardial oxygen consumption. The vasodilatory effect on large epicardial coronary arteries, especially on eccentric stenoses through relaxation of vascular smooth muscle tone was described even more recently (1980). This effect proved to be of considerable clinical importance both in angina at rest, that is during a primary increase in vasomotor tone (coronary artery spasm) as well as in angina provoked by exercise, where the increase in vasomotor tone and in the degree of stenosis is often due to a rise in alpha-sympathetic tone. The relaxing effect on the large coronary arteries is regarded as additive to the one on venous tone. The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. The tendency for coronary arteries to constrict in presence of atherosclerosis is explained by the lack of EDRF, especially in the region of atherosclerotic plaques where the endothelium is often absent or has lost its endocrine function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The mechanism of action of nitrates, 1988 status]. 251 90

Type II altitude-related decompression sickness (DCS), due to its wide spectrum of symptoms, is often difficult to diagnose. This difficulty sometimes leads unnecessarily to the permanent grounding of an experienced aviator. So that this condition could be better understood, a total of 133 cases of Type II altitude DCS (on file at the United States Air Force Hyperbaric Medicine Division, School of Aerospace Medicine, Brooks AFB, TX) were reviewed. Most cases (94.7%) followed altitude chamber training. The most common manifestation was joint pain (43.6%), associated with headache (42.1%), visual disturbances (30.1%), and limb paresthesia (27.8%). The next most common symptoms were, in order of decreasing frequency: mental confusion (24.8%), limb numbness (16.5%), and extreme fatigue (10.5%). Spinal cord involvement, chokes, and unconsciousness were rare (6.9%, 6%, and 1.5%, respectively). Hyperbaric oxygen treatment produced fully successful results in 97.7% of the cases. Only 2.3% of the cases resulted in residual deficit; no deaths occurred. A thorough knowledge of the differential diagnosis and predisposing factors is essential to narrow the margins of error in the diagnosis and prevention of decompression sickness in the operational or training environment. A recommendation for favorable consideration of waiver action for those aviators who suffered Type II DCS is presented. These recommendations are based on a unique classification of the severity of symptoms.
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PMID:Type II altitude decompression sickness (DCS): U.S. Air Force experience with 133 cases. 265 1

Respiratory insufficiency of any cause has significant effects on the nervous system. Headache, mental status changes, papilledema, and numerous motor abnormalities including asterixis are commonly seen. Abnormalities in ventilation and gas exchange result in hypoxia, hypercapnia, and respiratory acidosis, and these, in turn, interfere with cerebral metabolism, increase CBF, and may raise intracranial pressure. Chronic respiratory insufficiency can persist for many months with minimal neurologic symptoms, as numerous compensatory mechanisms, particularly renal, may take effect. Treatment includes restoring adequate ventilation and improving gas exchange and may require tracheal intubation and assisted ventilation. Supplemental oxygen therapy should be carefully monitored, as high rates of flow may suppress the hypoxic drive for respiration and lead to significant carbon dioxide retention. The sleep apnea syndromes are a group of disorders in which abnormal respiratory patterns during sleep result in hypercapnia and hypoxemia. Intermittent obstruction of the upper airway and abnormalities of brainstem respiratory centers cause frequent nocturnal awakenings and apneas in these patients. Treatments vary and include weight loss in obese subjects, respiratory stimulants, tracheostomy, and diaphragmatic pacing. Rapid ascent to high altitudes may result in headache, changes in mental status, papilledema, and other neurologic symptoms in certain individuals: a syndrome known as high-altitude sickness. Hypoxia leading to cerebral edema, nocturnal periodic breathing, and hypobaria produces neurologic symptoms in these individuals. Acetazolamide and dexamethasone may be effective in minimizing symptoms of this disorder. Sustained hyperventilation produces acral and circumoral paresthesias and lightheadedness in anxious individuals and can be maintained by relatively normal ventilatory patterns once established. These symptoms are due to hypophosphatemia and respiratory alkalosis, the latter reducing CBF and causing localized tissue hypoxia. Rebreathing into a paper bag at the first awareness of symptoms is the most effective form of treatment.
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PMID:Neurologic manifestations of pulmonary disease. 267 37

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

A patient with severe cluster headaches was treated in a hyperbaric chamber on two occasions. Her symptoms had been refractory to other treatment modalities including conventional oxygen therapy. On both occasions her pain was promptly relieved while breathing 100% oxygen at two atmospheres of pressure. This is the first known reported case of a cluster headache treated with hyperbaric oxygen. A prospective study is needed to substantiate the efficacy of this treatment modality for cluster headaches.
Headache 1989 Feb
PMID:Treatment of a cluster headache patient in a hyperbaric chamber. 270 39

Carbon monoxide poisoning causes tissue hypoxia because of reduced transfer and altered release of oxygen by hemoglobin. Considering many case histories, we realized that symptoms and clinical signs of acute poisoning are mostly neurologic: coma, headache, dizziness, vomiting. On the contrary, it seems that myocardium, the other organ which mostly requires O2, is attacked in a "silent way". ECG in 5 patients with accidental carbon monoxide poisoning underlined that cardiac rate increased (3 of them presented tachyarrhythmias by atrial fibrillation) and the presence of more or less important alteration of ventricular repolarization like "subendocardial lesion". Simple hyperbaric oxygen treatment determined the regression of the rhythm disorder and of the abnormalities of ventricular repolarization. The only patient who had not the restoration of sinus rhythm had chronic atrial fibrillation.
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PMID:[Cardiologic aspects of carbon monoxide poisoning]. 275 46


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