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

Twenty-two smokers with elevated hematocrits (mean, 54 per cent) had elevated blood carboxyhemoglobin (mean, 11.6 per cent; normal, less than 1 per cent) and a "left-shifted" oxygen-hemoglobin dissociation curve (mean P50, 21.6 +/- 2.3 [+/- S.D.] torr; normal, 26.7 +/- 1.1). Red-cell volume was increased in 14 of 18, and plasma volume reduced in 14 of 18. Fatigue and headache were common, and syncopal attacks occurred in four patients. Symptoms disappeared and the elevated red-cell volume decreased markedly in all five patients who were able to reduce severely their smoking habit; low plasma volume increased in three of four patients studied. We conclude that carbon monoxide exposure from cigar and cigarette smoke is a frequent cause of an elevated red-cell volume or a reduced plasma volume (or both). Measurement of carboxyhemoglobin should be a routine part of the evaluation of all polycythemic subjects.
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PMID:Smokers' polycythemia. 61 65

Three incidences of carbon monoxide poisoning occurred owing to defective heating systems. Twelve persons were affected; of these, three lost their lives. Because the symptoms of carbon monoxide poisoning closely resemble flu and other common illnesses, correct diagnosis was not made as promptly as it might have been. Hemorrhages were found in the nerve fiber layer of the retina in all five of the patients who had been exposed for more than 12 hours. It is our contention, therefore, that complete examination of the patient should always include ohthalmoscopy, and that the finding of retinal hemorrhages, in addition to nausea, headache, and dizziness, should aler the physician to the possibility of carbon monoxide poisoning.
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PMID:Retinal hemorrhages in subacute carbon monoxide poisoning. Exposures in homes with blocked furnace flues. 63 61

In industrial countries the symptoms "headache" has an incidence of about 10%, and hypertension between 20 and 25%. Both terms are summary and may be pointers to and warning signals of the most varied disease processes. While, in malignant hypertensions, and pheochromocytoma, headache is a cardinal symptom, its causal connection with permanently raised blood pressure in the "benign" forms is viewed with scepticism. The observation that hypertensives frequently complain of headaches with a maximum intensity in the early hours of the morning is connected with the fall in blood pressure with accumulation of CO2 in shallow breathing. Headache as a symptom characteristic of hypertension is frequently only facultative in nature and must be classified among the series of symptoms of sequelae. But it offers a sufficient reason to institute a selective examination programme, especially as hypertension is still the most common cause of death even today.
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PMID:[Headache associated with hypertension from the internist's and neurologist's point of view (author's transl)]. 81 25

A case of primary Intracranial Hypotension (PIH) is described. This syndrome consists of spontaneous lowering of CSF pressure with traction headache. It is a benign disorder and is self-limited. The cause is unknown, but local choroid plexus vasospasm, possibly due to a hypothalamic disturbance, has been suggested, as has leakage of CSF through spontaneous arachnoid tears. Transient symptomatic relief was achieved with 5% CO2 inhalation, apparently due to increase in cerebral blood flow.
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PMID:Primary intracranial hypotension: the syndrome of spontaneous low cerebospinal fluid pressure with traction headache. 83 25

A syndrome of alveolar hypoventilation has been identified in a group of patients with bilateral diaphragm paralysis. Eight patients were studied in whom diaphragm weakness had been suggested by paradoxical (inward) movement of the abdominal wall on inspiration, of whom seven had evidence of a generalized neuromuscular disorder. Diaphragm function was assessed quantitatively by measurement of the change in transdiaphragmatic pressure during a maximum inspiration (deltaPDi). In five patients, deltaPDi was zero and in the others ranged from 2-6 cm H2O (normal greater than 25 cm H2O) indicating paralysis and severe weakness in the respective groups. Fluoroscopy of the diaphragm was found to give misleading results, and the resons for this are considered. Vital capacity ranged from 65-30 per cent of the predicted normal in the upright posture, typically falling by about a half in the supine posture. Alveolar hypoventilation was present in five patients when supine and in six when asleep, the deterioration in blood gases associated with sleep generally being much greater in these patients than in normal subjects. Respiratory rate was significantly greater than age-matched controls. The ventilatory response to CO2 was impaired. The PCO2 could be brought to normal levels by voluntary hyperventilation, and the unreliability of voluntary respiratory manoeuvres of this kind as indices of ventilatory reserve is emphasized. Alveolar hypoventilation was associated with disturbed sleep, morning headache and day-time fatigue. Symptomatic benefit was achieved by the use of a cuirass respirator at night.
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PMID:Diaphragm function and alveolar hypoventilation. 106 15

Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & Therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.
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PMID:Management of the moribund carbon monoxide victim. 811 Mar 42

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

In this study, blood flow velocity in the basilar artery and both vertebral and middle cerebral arteries was measured with a transcranial Doppler device in 23 migraineurs during and outside a migraine attack. The aim of the study was to compare blood flow velocities during and outside an attack and to examine vascular reactivity to voluntary hyperventilation during both conditions. No differences in blood flow velocity were found. Although blood pressure was increased and end-expiratory CO2 decreased during the attack, this exerted no influence on blood flow velocity. Neither was a difference in vascular reactivity to voluntary hyperventilation detected between the two conditions. These findings support the notion of functional integrity of the examined large arteries during migraine attacks without aura.
Cephalalgia 1992 Feb
PMID:Blood flow velocities in the vertebrobasilar system during migraine attacks--a transcranial Doppler study. 155 55

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

Post-polio patients sometimes complain about the occurrence of breathing difficulties decades after the polio infection. We have examined 40 post-polio patients who have had respiratory or non-respiratory poliomyelitis for at least 30 years in an attempt to elucidate whether hypoventilation is common and to what extent certain symptoms and simple lung function tests are related to hypoventilation or incipient hypoventilation. We measured arterial blood gases, vital capacity (VC), maximal expiratory and inspiratory pressures (MEP, MIP) and CO2 rebreathing response. Symptoms were assessed by a yes/no questionnaire. Six patients required respiratory assistance at the onset of the disease. At present, two require nocturnal assisted ventilation. Two patients showed manifest hypoventilation; one of which required night-time ventilator, whereas the other patient had not required ventilatory assistance even at the onset of the disease. Significant correlation (p less than 0.05) was found between arterial carbon dioxide tension (a-PCO2) and VC, MEP and ventilation increase during CO2 rebreathing. A significantly higher a-PCO2 was found among those who required respiratory assistance at the onset of the disease, who admitted headache and who felt the cough ineffective. Low VC and low ventilatory increase during CO2 rebreathing and the presence of headache explained 45% of the variation in a-PCO2 in a multiple regression analysis. We conclude that manifest hypoventilation is rare in this unselected material of post-polio patients and that a vital capacity below 45-50% of predicted normal and the presence of frequent headaches indicate an increased risk to develop hypoventilation.
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PMID:Post-polio lung function. 160 61


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