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

Symptoms of carbon monoxide poisoning in a nonsmoking patient continued for several years until her husband stopped smoking cigarettes near her. Carbon monoxide poisoning should be considered in non-smokers when characteristic toxic symptoms occur (ie, lethargy, irritability, headache, blurred vision, slowed reaction time, and decreased concentration). Toxicity may develop simply from breathing second-hand smoke.
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PMID:Secondhand cigarette smoke as a cause of chronic carbon monoxide poisoning. 724 2

Low formaldehyd-concentrations were measured in three Cologne schools (mean 1 = 0,4425; mean 2 = 0,5725; mean 3 = 0,1292 ppm). As the main sources of emission were identified formaldehyd-urea-bound chip-plates in acoustic-ceilings and wainscots. To study the connection between the complaints of pupils and CH20-emissions 1594 pupils of these schools were questioned using a specially elaborated questionnaire. The questions concerned multiple complaints and disturbances of health as well as their anamnesis in chronological relationship with school attendance. Compared to controls consisting of 497 pupils of a school, where no CH2O-emitting chip-plates were used, the inquiry showed a significant increase (p less than 0,00005) of so-called functional disturbances (headache, disorder of concentrating ability, dizziness, nausea), affections of the respiratory tract (irritation of the mucosa of the nose and the pharynx, dry cough) and irritation of the conjunctiva. In regard to the anamneses, the difference between the investigation-group and the control-group was even more significant and additional complaints such as somnipathy, abdominal pain, skin disease were observed frequently. Comparing the normal distribution of so-called functional disturbances in pupils found in literature, the examined group of this study showed an even higher rate of the relative accumulation. The repeated investigation in one school (n = 328) 8 months after removal of the emission-sources demonstrated a very clear reduction of complaints by an average of 71,2 per cent.
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PMID:[Damages to health in schools. Complaints caused by the use of formaldehyde-emitting materials in school buildings]. 737 30

By providing a non-invasive method for continuous display of mean flow velocity (Vmean) in the cerebral arteries, transcranial Doppler (TCD) ultrasound supplements evaluation of cerebral perfusion. Dynamic exercise increases middle cerebral artery (MCA) Vmean from approximately 55 to 65 cm s-1 dependent on work rate, and even more when corrected for changes of the arterial carbon dioxide tension. Evaluation of Vmean corresponds to that of cerebral blood flow as determined with the 133Xenon clearance technique, and reflects regional cortical regulation of the active muscles with important afferent nervous influence. Concomitant increases of mean arterial pressure (MAP) and heart rate is only of minor importance as illustrated during static exercise and post-exercise muscle ischaemia, where Vmean is not significantly elevated. During sustained head-up tilt, the Vmean remained unchanged at a MAP approximately 83 mmHg. Below this level, it decreased in parallel with MAP until MAP reached 50 mmHg. At an even lower MAP, Vmean seemed to approach a lower limit approximately 25 cm s-1, but at a diastolic pressure of 21 mmHg there was no flow in the MCA. Conversely, during post-exercise muscle ischemia, an increase in MAP to 140 mmHg did not influence Vmean. This is in contrast to patients operated for carotid artery stenosis and who develop ipsilateral headache. In these patients the ipsilateral MCA Vmean changed in parallel with MAP, and autoregulation was re-established only after one to two weeks. In patients with severe carotid stenosis and poor collateral circulation, the CO2-reactivity as expressed by Vmean was the lowest, and could be negative on the ipsilateral side. During carotid endarterectomy, a Vmean clamp/Vmean pre-clamp ratio below 0.6 identified patients with a cerebral blood flow below 20 ml 100 g-1 min-1. Furthermore, when the ratio was below 0.4 pathological electroenchephalographic changes developed. Thus, Vmean of the large basal cerebral arteries reflects cerebral perfusion with respect to regional flow distribution, autoregulatory response, and CO2-reactivity in normal man and patients with limited cerebral flow.
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PMID:Transcranial Doppler ultrasound for cerebral perfusion. 748 67

Some controversial issues exist whether regional cerebral blood flow (rCBF) changes are present both in migraine with and without aura during the interictal period. For this reason we have studied rCBF characteristics in migraine patients when headache-free. rCBF examinations were performed by the 133Xe inhalation method on 39 normal subjects (24 aged 45 or less and 15 older than 45), on 10 migraine patients with (A+) and on 10 without (A-) aura. The values of each patient were compared with the age-matched control population mean by a computer-assisted mapping system that allows statistical analysis in real time. To compare inter-individual variability 10 subjects, out of 39 normals, constituted an age-, sex- and CO2-matched control group (C). 8 A+ patients and 7 A- showed significant alterations of CBF in comparison with the age-matched control population. The analysis between the age-, sex- and CO2 matched groups showed significant differences of the inter-hemispheric (F = 6.669, p = 0.004) and of the frontal (F = 7.480 p = 0.0008) asymmetries. These data show that in the headache-free period a derangement of the cerebral perfusion is present in both migraine with and without aura, suggesting they are due to the same disease process. Furthermore they show the usefulness of a computer-assisted mapping system, suitable for clinical use, in discovering small alterations in cerebral perfusion.
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PMID:Interictal abnormalities of regional cerebral blood flow in migraine with and without aura. 756 59

Dietary cells and the vitamins B12 and folate are necessary for the production of the red blood cells (erythrocytes), which carry oxygen from the lungs to the tissues and carbon dioxide from tissues to lungs. Deficiency of either one results in anaemia, which is characterised by low haemoglobin concentration. Symptoms result from reduced tissue oxygenation and include weakness, lethargy, palpitation, headache and shortness of breath. The first-time laboratory test of all patients suspected of being anaemic is the full blood count. Results of a full blood count may suggest the anaemia is caused by a nutritional deficiency of B12 folate or iron. Laboratory measurement of the concentration in blood of iron and vitamin B12 and folate, along with several other tests described here, are useful in the differential diagnosis of the anaemic patients.
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PMID:Deficiency testing for iron, vitamin B12 and folate. 760 52

Seven SUNCT patients (six men, one woman) took part in this study. In four patients, respiratory variables were compared during and outside attacks. In five patients, peripheral chemosensitivity was tested and compared with a control group matched with respect to age, sex, and smoking habits. The results indicate that SUNCT patients hyperventilate during attacks. Moreover, they appear to hyperventilate slightly under basal conditions. The tests for peripheral chemoreceptor activity indicated no differences between the SUNCT and the control groups except for one variable, namely the mean ventilatory response to a single breath of 13% CO2. It is possible that this indicates a blunted response of the peripheral chemoreceptors. On the other hand, it may also represent a chance finding, since none of the other results presented suggested such a conclusion, and the size of the test group was very small. The results do not indicate that a reduction in oxygen saturation can trigger SUNCT since low levels of oxygen saturation were only rarely accompanied by SUNCT, whereas many attacks were not associated with any appreciable lowering in arterial oxygen saturation.
Headache 1995 Jun
PMID:Respiratory studies in SUNCT syndrome. 763 20

Carbon monoxide poisoning usually results from inhalation of exhaust fumes from motor vehicles, smoke from fires or fumes from faulty heating systems. Carbon monoxide has a high affinity for hemoglobin, with which it forms carboxyhemoglobin. The resulting decrease in both oxygen-carrying capacity and oxygen release can lead to end-organ hypoxia. The clinical presentation is nonspecific. Headache, dizziness, fatigue and nausea are common in mild to moderate carbon monoxide poisoning. In more severe cases, tachycardia, tachypnea and central nervous system depression occur. When carbon monoxide intoxication is suspected, empiric treatment with 100 percent oxygen should be initiated immediately. The diagnosis is confirmed by documenting an elevated carboxyhemoglobin level. Hyperbaric oxygen therapy is recommended in patients with neurologic dysfunction, cardiac dysfunction or a history of unconsciousness.
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PMID:Carbon monoxide intoxication. 769 50

Medical directors of North American hyperbaric oxygen (HBO) facilities were surveyed to assess selection criteria applied for treatment of acute carbon monoxide (CO) poisoning within the hyperbaric medicine community. Responses were received from 85% of the 208 facilities in the United States and Canada. Among responders, 89 monoplace and 58 multiplace chamber facilities treat acute CO poisoning, managing a total of 2,636 patients in 1992. A significant majority of facilities treat CO-exposed patients with coma (98%), transient loss of consciousness (LOC) (77%), ischemic changes on electrocardiogram (91%), focal neurologic deficits (94%), or abnormal psychometric testing (91%), regardless of carboxyhemoglobin (COHb) level. Although 92% would use HBO for a patient presenting with headache, nausea, and COHb 40%, only 62% of facilities utilize a specified minimum COHb level as the sole criterion for HBO therapy of an asymptomatic patient. When COHb is used as an independent criterion to determine HBO treatment, the level utilized varies widely between institutions. Half of responding facilities place limits on the delay to treatment for patients with only transient LOC. Time limits are applied less often in cases with persistent neurologic deficits. While variability exists, majority opinions can be derived for many patient selection criteria regarding the use of HBO in acute CO poisoning.
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PMID:Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. 777 95

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

Ten patients with cluster headache in an active period and 6 controls were studied as to heart rate, blood pressure, blood flow in the common carotid arteries (CCA), end-tidal PCO2 and pain before, during and after 6 minutes of breathing 6% CO2 in air. Heart rate increased significantly during CO2 breathing in controls but not in patients. The cluster headache patients had significantly lower baseline end-tidal PCO2 than controls. CCA blood flow increased significantly during CO2 breathing in both groups. Vascular resistance decreased during CO2 provocation and increased above baseline levels 5 minutes after provocation in both groups and related to the end-tidal PCO2. Six of eight cluster headache patients, who had an increase of blood flow at provocation, reported slight to moderate unilateral pain in relation to the CO2 provocation in contrast to controls. One patient treated with 6 mg sumatriptan 2.5 hours before the provocation had an end-tidal PCO2 within the range of the controls, and did not get an increase of CCA blood flow or pain at provocation. Six of the cluster headache patients were restudied when out of the active period. There was still no heart rate increase during CO2 breathing and end-tidal PCO2 was still lower than in the controls. Unilateral headache was not provoked.
Headache 1995 Jan
PMID:Provocation of unilateral pain in cluster headache patients by breathing CO2. 786 33


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