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

To investigate occult carbon monoxide poisoning in patients with neurologic illness, we prospectively studied 168 patients who presented to the emergency department between December 1987 and February 1988 with neurologic symptoms for evidence of carbon monoxide exposure. Patients with known carbon monoxide poisoning were excluded. The mean carboxyhemoglobin level was 3.1 percent; there were no significant differences in carboxyhemoglobin between categories of neurologic illness (F(5,162) = 1.35; p less than 0.25). Five patients (3 percent) had a carboxyhemoglobin greater than 10 percent, with levels ranging from 11.7 percent to 29.5 percent. After controlling for the effects of active and passive exposure to cigarette smoke, problems with the home heating system (odds ratio 9.6; p less than 0.03) and the presence of cohabitants with concurrent headache or dizziness (odds ratio 21.6; p less than 0.0001) were associated with an increased risk of a carboxyhemoglobin greater than 10 percent. A rule for obtaining carboxyhemoglobin tests only on patients who used gas stoves for heat or who had symptomatic cohabitants would have correctly identified all patients with carboxyhemoglobins greater than 10 percent, correctly excluded 77 percent of patients with lower levels, and eliminated the need for testing in 75 percent of cases. We conclude that unrecognized carbon monoxide poisoning occurs in a small but important fraction of patients with wintertime neurologic illness and can be identified by a characteristic risk factor profile.
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PMID:Occult carbon monoxide poisoning in patients with neurologic illness. 238 Oct 21

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

Diesel motors are employed to an increasing extent for occupational transport and fumes from diesel driven vehicles constitute an increasing problem as regards atmospheric pollution but, in particular, they constitute a considerable risk to health for the workers exposed to diesel exhaust fumes in their daily work. In the clinic for occupational medicine, The University Hospital, Copenhagen, 14 garage workers were examined. Eleven of these had been exposed to great quantities of diesel exhaust fumes for 2 to 29 years. All 11 presented acute symptoms due to diesel exhaust fumes in the form of headache, vertigo, fatigue, irritation of mucous membranes, nausea, abdominal discomfort or diarrhoea. Seven persons had been employed for more than five years as garage workers. Six complained of failure of memory, difficulty in concentration, irritability, increased sleep requirement, psychological changes or reduced libido. Neuropsychological examination was undertaken in these six persons and in five of them organic brain damage, mainly of slight extent, was demonstrated. Diesel exhaust fumes contain many toxic substances: carbon monoxide, nitrous gases, sulphur oxides, aldehydes and hydrocarbons. It is not possible to indicate a single compound which is responsible for possible brain damage and a combination effect may well be concerned. This is a casuistic material. Only few investigations have previously been available which illustrated a possible connection between the neurotoxic effects and, in particular, brain damage. It is now considered important to emphasize that this may constitute a problem on exposure to diesel exhaust fumes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Organic brain damage in garage workers after long-term exposure to diesel exhaust fumes]. 247 26

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

The authors describe the case of a 37-year-old patient, who, after a minor craniocerebral trauma suffered in 1970, was admitted to hospital because of progressive headache, unsteady gait and balance disturbances, deglutition disorders and diplopia. Computed tomography (CT) scan showed a large median hyperdense tumour of posterior fossa with the fourth ventricle involvement. Operation under microscope was performed to remove a considerably large cystic tumour, occupying the fourth ventricle and cisterna magna, displacing the cerebellar lobes and pushing the vermis upward. The tumour was waxy and grey, whereas the cystic liquid had the colour and consistency of oily fluid. The capsule was occluded with the CO2 laser. Postoperative course was good.
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PMID:Dermoid tumour of the fourth ventricle with hyperdense aspect demonstrated on CT scan. Case report. 258 31

The side-effects of two opioid agonist-antagonists, nalbuphine and pentazocine, were assessed when used for patient-controlled postoperative analgesia. Forty ASA I or II patients scheduled for upper abdominal surgery were randomly allocated to two equal groups. The anaesthetic technique was the same for all the patients: premedication with atropine and diazepam, induction with thiopentone and suxamethonium and maintenance with fentanyl, pancuronium, nitrous oxide and halothane. Patient-controlled computer assisted analgesia (On-Demand Analgesia Computer) was started in the recovery room at least 2 h after the last administration of fentanyl. The parameters used were: a routine hourly dose (the half of that received during the previous hour), with on demand delivery of nalbuphine (15 micrograms.kg-1) or pentazocine (45 micrograms.kg-1) aliquots respectively, with a refractory period between two demands of 4 min and a total hourly maximum dose of 16 mg and 48 mg respectively. The following parameters were measured before the start of self-administration, and every hour afterwards for 24 h: systolic (Pasys) and diastolic blood pressures, heart rate, pressure-rate product (PRP), respiratory rate, end-tidal CO2 and pain (by way of a three point scale). Analgesia was assessed on a four-point scale every 6 h. The total doses of nalbuphine and pentazocine administered were 94 +/- 43 mg and 251 +/- 150 mg respectively. The only parameters significantly different between the two groups were Pasys and PRP, being higher in the pentazocine group. There were no significant differences in the side-effects (drowsiness, nausea, vomiting, headache, amnesia, logorrhoea and urine retention). All patients in both groups were satisfied with this technique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of nalbuphine and pentazocine in the treatment of postoperative pain by self-administration]. 266 Jun 40

Regional cerebral blood flow (CBF), mood states and somatic symptoms were measured before and after inhalation of amyl nitrite in 10 physically healthy volunteers with a prior history of using volatile nitrites for recreational purposes. CBF was measured with the same technique, under identical laboratory conditions, in an equal number of normal volunteers. During CBF measurements, blood pressure, pulse rate, respiratory rate and end-tidal levels of carbon dioxide were monitored. The amyl nitrite group and the control group were compared on CBF, rating scale scores and physiological indices via analysis of variance. Amyl nitrite inhalation was associated with significant global increases in CBF, while the control group did not show any change. Pulse rate increase was the only physiological change associated with administration of the drug. Subjects who received the drug reported significant decrease in anger, fatigue and depression and increased palpitation, breathing difficulty, dizziness and headache. Changes in the rating scale scores, physiological indices, and somatic symptoms after amyl nitrite did not correlate with regional CBF change.
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PMID:Regional cerebral blood flow changes associated with amyl nitrite inhalation. 270 85

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

The ferrihaemoglobin (HbFe3+) formation by amyl nitrite (AN) or sodium nitrite (NaNO2) was studied in different species including man, in vivo and in vitro. In in vivo studies AN was administered intravenously (i.v.), intramuscularly (i.m.), by inhalation, or orally. NaNO2 was injected i.v.. AN i.v. produced HbFe3+ much more rapidly than NaNO2 in dogs, cats, rabbits, and rats. In dogs, i.m. injection of AN was followed by a very slow linear increase in the HbFe3+ content. Inhalation of AN did not lead to HbFe3+ formation in dogs unless it was rebreathed in a closed (bag) or not completely open (gas mask) system. HbFe3+ was produced by oral AN in dogs, the effect being enhanced by addition of DMSO. Inhalation of AN by human volunteers in a gas mask and from ampoules crushed close to the nose did not induce haemoglobin oxidation to a practically significant extent, but it was associated with headache, tiredness, dizziness, and a fall in blood pressure. In in vitro studies, in contrast to NaNO2, AN produced HbFe3+ instantaneously in erythrocytes of various species and in purified human haemoglobin. AN 1 mol yielded 2 mol Fe3+. Only 20% of the oxygen released during the oxidation of haemoglobin by AN or NaNO2 was recovered. In 0.2 M phosphate buffer, pH 7.4, 0.01 mol O2/mol AN was consumed. CO2 was released in the presence of AN, but not of NaNO2, from blood, plasma, and 0.02 M NaHCO3 solution. The ratio (lactate)/(pyruvate) decreased when HbFe3+ was formed by AN or NaNO2.
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PMID:Ferrihaemoglobin formation by amyl nitrite and sodium nitrite in different species in vivo and in vitro. 290 49

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


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