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

Arteriovenous malformations (AVM) are congenital vascular lesions consisting of direct communications between associated arteries and veins without an interposed capillary bed. These vessels are typically thin walled, lack an internal elastic intima, and are quite prone to hemorrhage. A previously healthy 17-year-old woman presented with severe, persistent headache. After undergoing computed tomography (CT scan) and magnetic resonance imaging (MRI), the patient was diagnosed as having an intracranial arteriovenous malformation. The anesthetic management of this patient included induction with sodium thiopental and sufentanil. General anesthesia was maintained with isoflurane in oxygen and a continuous intravenous infusion of sufentanil. Neuromuscular blockade was established prior to endotracheal intubation with vecuronium and maintained with a combination of metocurine and pancuronium. The sufentanil infusion was discontinued when vascular isolation of the AVM had been accomplished. The isoflurane was discontinued 30 minutes prior to skin closure. Neuromuscular blockade was then antagonized with neostigmine and glycopyrrolate. Spontaneous ventilation resumed when the patient's arterial carbon dioxide tension (PaCO2) was allowed to normalize. The hemodynamic character of this anesthetic course was smooth and uneventful. The patient emerged from anesthesia comfortable and lucid and experienced no perioperative anesthetic complications.
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PMID:Excision of an arteriovenous malformation. 195 Apr 4

A 25-year-old patient with headache was admitted to the neurology department. Computerized tomography revealed an intracerebral abscess of unknown origin, which was removed by craniotomy. After an uneventful operation and anesthetic low arterial oxygen tensions were noted that did not respond to increased FiO2. Angiography revealed a pulmonary arteriovenous (a-v) fistula (angioma), which was responsible for the right-left shunt. A Swan-Ganz catheter was inserted and the effects of varying levels of PEEP on the magnitude of the shunt during spontaneous breathing of 100% oxygen were determined. At zero PEEP the arterial pO2 was 211 mm Hg (AaDO2 470 mm Hg). 5 mbar PEEP caused the arterial pO2 to fall to 118 mm Hg (AaDO2 563 mm Hg). Increasing PEEP to 15 mbar caused a further decrease in arterial pO2 to 72 mm Hg (AaDO2 603 mm Hg), which resulted in arterial desaturation. The arterial pCO2 remained constant. At a virtually constant cardiac output the shunt volume increased from 23% at zero PEEP to 30% at a PEEP of 15 mbar--a relative increase of 30%. Elevating the intrathoracic pressure presumably caused redistribution of the pulmonary perfusion toward the shunt vessels, probably because the vascular resistance increased more rapidly in the normal vasculature than in the angioma. The therapeutic consequences were to reduce the PEEP and avoid mechanical ventilation. Pulmonary a-v-fistulas are not uncommonly associated with brain abscesses, probably because the normal filter function of the pulmonary vascular bed is disrupted. Therapy consists either in resecting the afflicted lung segment or in transvenous occlusion of the fistula with a silicon ballon.
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PMID:[Deterioration of pulmonary gas exchange caused by PEEP in a pulmonary vascular shunt (Rendu-Osler-Weber syndrome)]. 203 23

Values for local cerebral blood flow (LCBF) were measured in three dimensions utilizing xenon enhanced computerized tomography among patients during spontaneously occurring cluster headaches, during headache-free intervals and immediately after terminating attacks by inhalation of 100% oxygen. Results were compared with values measured among age-matched normal volunteers. LCBF values measured in five cluster patients while headache-free did not differ from similar measures among age-matched normal volunteers. In three patients during attacks of spontaneously occurring cluster headache, LCBF values for temporal cortex, basal ganglia and subcortical white matter were increased. Immediately after terminating attacks of cluster by 100% oxygen inhalation for five minutes, LCBF values for temporal cortex and basal ganglia became significantly decreased below normal values in five patients with spontaneously occurring cluster headache. Prompt relief of head pain by inhalation of 100% oxygen is associated with abolition of the hyperperfusion of both cortical and subcortical brain structures that occurs during spontaneously occurring cluster headaches and is followed by excessive cerebrovascular constriction. It remains to be determined whether the cerebral hyperemia occurring during cluster headaches is causally related to the head pain or is secondary to the pain itself. Rapid termination of head pain by hyperoxia associated with excessive cerebral vasoconstriction suggests that this vascular phenomenon is unique to cluster headache and offers clues to its pathogenesis.
Headache 1991 Apr
PMID:Cerebral hyperemia during spontaneous cluster headaches with excessive cerebral vasoconstriction to hyperoxia. 205 May 16

The effect of voluntary hyperventilation was assessed in 22 cluster headache patients (8 in a cluster period and 14 in a remission) and 19 healthy individuals. Using an ear oximeter and a capnograph with a nasal probe, the oxygen saturation (SaO2) and the end-tidal CO2 were monitored continuously. During the hyperventilation per se, cluster headache patients and controls showed absolute values of end-tidal CO2 and of SaO2 of the same order of magnitude. In the posthyperventilation phase, however, the average of the lowest SaO2 levels was lower in controls than in cluster headache patients. In the posthyperventilation phase, headache patients outside the cluster period showed a trend more similar to that of the controls with respect to SaO2 than did those inside the cluster period. The observed discrepancy might, if reproducible, be a consequence of an altered chemoreceptor sensitivity in cluster headache patients during the bout.
Headache 1991 Mar
PMID:The effect of hyperventilation in cluster headache patients. 207 91

An association exists between bruxism, tension headache, and sleep disorders, particularly sleep apnea, in the craniomandibular dysfunction patient. Understanding the relationship of these three entities provides the clinician with valuable information that enhances one's ability to make a differential diagnosis. A review of sleep disorders is presented so that a clearer understanding of them can be gained, with emphasis on obstructive sleep apnea. Current theories regarding bruxism, morning headache, and sleep disorders relate closely to altered muscle activity, altered breathing and fluctuation in oxygen saturation levels, which in turn can contribute to a patient's complaints of various types of facial pain.
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PMID:Tension headache and bruxism in the sleep disordered patient. 207 98

Acute mountain sickness is a pathologic reaction as a result of bad adaptation to high altitudes (greater than 2.500 meters). The main symptoms are headache, nausea, vomits, and insomnia. When severe it can produce oliguria, retinal hemorrhage, ataxia and sometimes coma. Its etiology is not well known. It is considered that the first producer factor of the disease is tissular hypoxia secondary to low partial oxygen pressure existing in areas of high sea level. The treatment consists of descent and the use of dexametasone and acetazolamide.
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PMID:[Acute mountain sickness]. 210 53

Ten episodic cluster headache patients in their active cluster period, ten patients in remission and five control subjects were monitored for minute to minute changes in oxygen saturation (SaO2) and pulse rate before and after nitroglycerin (NTG) administration. A transient but significant decrease in SaO2 and increase in pulse rate of 25 minutes duration occurred following NTG in all groups. These changes may reflect physiologic hemodynamic effects of NTG as a smooth muscle relaxant. Subsequently, SaO2 levels and pulse rate recovered to baseline values in remission and control groups. In contrast, SaO2 values in the active cluster group decreased further and after an extended period culminated in cluster headache attacks in 10/10 patients. Three major changes, therefore, distinguished active cluster patients from remission and control groups. First, the magnitude of oxygen desaturation increased after the physiological effects of NTG ceased. Second, oxygen desaturation was sustained for an additional 9 to 30 minutes duration. Third, the hypoxemic state culminated in attacks in all cases. Our findings suggest that the active cluster period may be characterized by an impaired mechanism to autoregulate, and thus compensate, for hypoxemia. It is further proposed that persistence of hypoxemia and the cluster attack onset may share a common mechanism, coupling the two events. We suggest that abnormal central and/or peripheral chemoreceptor activity may be responsible for these events.
Headache 1990 Jul
PMID:Association of sustained oxyhemoglobin desaturation and onset of cluster headache attacks. 212 67

Prolonged (several days or repeated) exposure to nitrous oxide (N2O) can cause injury or death. To assess whether relatively prolonged anesthesia with N2O in normal patients might similarly cause untoward effects, we investigated whether the addition of N2O to isoflurane anesthesia caused injury to patients having surgical resection of acoustic neuroma lasting approximately 10 h. Twenty-six patients undergoing surgical resection of acoustic neuroma were randomly assigned to a regimen that included or excluded N2O (50%-60%) during isoflurane anesthesia plus intravenous adjuvants. On average, slightly less isoflurane (0.24%) was used during anesthesia with N2O. We measured standard clinical variables (blood pressure, heart rate), oxygen saturation, neurologic status, pain, and the incidence and type of morbid outcomes. Exposure to N2O did not increase the incidence of morbid outcomes (including hepatic injury, infection, or hypoxemia), prolong hospitalization, or increase common postoperative complaints such as nausea, vomiting, coughing, or headache. Patients anesthetized with either regimen were equally satisfied with their anesthetic.
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PMID:Effect on outcome of prolonged exposure of patients to nitrous oxide. 224 Jun 28

Two cases of cerebral malaria with hyperkinetic shock are reported. The first case concerned a 39-year-old european male who was not taking any prophylactic anti-malarial drugs. After having had headache and fever for a week, he was admitted to the intensive care unit (ICU) in coma and with jaundice. His initial systolic blood pressure was 60 mmg, with a central venous pressure (CVP) of -3 cmH2O. Five-hundred ml of modified fluid gelatin increased the CVP without raising the blood pressure. Haemodynamic investigations revealed a cardiac index (CI) = 5.2 l.min-1.m-2, peripheral arterial resistances (Rsa) = 290 dyn.s.cm-5, oxygen consumption (VO2) = 120 ml.min-1.m-2. Despite treatment with dopamine and dobutamine, the patient died 3 h after his admission, with a CI of 1.9 l.min-1.m-2. The second patient was a 14-year-old senegalese girl, admitted in circumstances similar to the first case. Initial haemodynamic investigations gave the following figures: CI 6.5 l.min-1.m-2, Rsa = 476 dyn.s.cm-5, VO2 = 174 ml.min-1.m-2. Recovery was obtained with fluid replacement therapy and dopamine. In the absence of another associated infectious disease, the plasmodial origin of the septic shock would seem to be the most likely in both cases. Pathophysiological mechanisms of these algid forms of malaria remain enigmatic. Various factors are discussed: cytoadherence of erythrocytes infected with Plasmodium falciparum, immunological disturbances, or a specific endotoxin.
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PMID:[Hyperkinetic shock and cerebral malaria]. 224 Jul

The present study concerns the possible relationship between hypoxia and the generation of cluster headache attacks. Fifteen controls and 25 cluster headache patients were studied. The patients were allocated into two groups according to cluster headache stage, i.e. cluster or remission period. During the tests, all the subjects were asked to inhale 12% oxygen (88% N2) for 30 min, and the decreasing oxygen saturation (SaO2%) was monitored. Patients in the remission period showed nearly the same decrement of SaO2% as controls. At the end of the test, patients in the bout showed significantly less reduction of SaO2% than the controls. In 5 patients, the test was carried out both in and outside the cluster periods. The tendency to less decrement in oxygen saturation in the cluster phase was as marked with this comparison, but the difference between the groups was not significant, probably partly due to the low number of tests carried out. Only one patient got a typical attack. It seems that hypoxia of this magnitude per se is not the cause of attacks. The different pattern with respect to SaO2% following 12% O2 inhalation in cluster headache may be due to an abnormality in central regulation and/or chemoreceptor sensitivity.
Headache 1990 Oct
PMID:Cluster headache: the effect of low oxygen saturation. 203 74


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