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

Phenylethylamine can initiate migraine-type headaches in susceptible individuals. Migraine sufferers have a reduced ability to deaminate all monoamines, but particularly phenylethylamine. Phenylethylamine readily crosses the blood-brain barrier and thus could be a mediator of the cerebrovascular disturbances seen in migraine attacks. Cerebral blood flow was measured in 15 anesthetized baboons by the intracarotid 133Xe clearance technique. Phenylethylamine (4 x 10(-7) moles.kg-1min-1) produced significant increases in cerebral blood flow (36 percent) and cerebral oxygen consumption (45 percent) during the first 40 minutes of infusion. In contrast, an increased phenylethylamine concentration (2 X 10(-6) moles.kg-1min-1) constricted the cerebral bed (cerebral blood flow reduced by 28 percent). The response of the cerebral circulation to hypercapnia was preserved during the infusion. Phenylethylamine thus is capable of producing in an experimental animal a pattern of cerebrovascular events similar to those seen in migraine.
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PMID:Phenylethylamine and cerebral blood flow. Possible involvement of phenylethylamine in migraine. 40 34

A case of brain abscess in the right parietal lobe secondary to pulmonary arteriovenous malformation of the right lung is presented. A 27-year-old man was admitted for headache and left homonymous hemianopsia. CAG, VAG and brain scan detected brain abscess of the right parietal lobe which was successfully removed surgically. He had been noted to have generalized cyanosis and club finger which corresponded to polycytemia and hypercapnia on examination. Subsequently pulmonary arteriovenous malformation was found in the right lower lobe of the lung which was also successfully excised by thoracic surgeons. Brain abscess was caused by peptostreptococcus anaerobius.
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PMID:[Brain abscess secondary to pulmonary arteriovenous malformation, case report (author's transl)]. 98 96

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

From this and the previous article, the following points may be offered in summary: When comparing the elderly age group with the general population, the incidence of migraine headaches decreases with age, whereas other etiologies such as glaucoma, temporal arteritis, and cerebrovascular disease may assume a more prominent role in the differential diagnosis. Patients in the geriatric population are frequently taking a multitude of medications, and it is extremely important to carefully evaluate these for possible precipitants of headache. Furthermore, in elderly patients with other potential medical problems, particular attention should be paid to the possibility of various systemic causes of headache. Therapy for specific headache disorders should be tailored to the individual patient. Consider the patient's overall general, psychological, medical, and neurologic background. The physician must be aware of possible interactions of medications with the therapeutic intervention, as well as possible poor tolerance to specific medications due to preexisting medical or neurologic disorders. A complete history, obtaining information on the temporal pattern of headache, the distribution of pain, and precipitating and alleviating factors, is extremely important in evaluating the elderly patient. A careful physical examination, paying particular attention to possible disorders of extracranial structures, is indicated. A neurologic exam, including basic tests of higher cortical function, should be obtained. Important additional laboratory investigations include a complete blood count, erythrocyte sedimentation rate, and basic blood chemistries. Arterial blood gases should be obtained in patients who have pulmonary disease, a history suggestive of sleep apnea, or other disorders that may produce hypoxia and hypercarbia, resulting in vascular headache.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Headaches in older patients: Ddx and Tx of common nonvascular causes. 405 33

This report describes a patient with primary alveolar hypoventilation who, after 2 yr of successful treatment with nocturnal oxygen, developed severe hypoxemia and hypercapnia during sleep, morning headaches, and daytime fatigue. Sleep studies demonstrated prolonged periods of hypoventilation and apnea without evidence of upper airway occlusion. Therefore, a phrenic nerve stimulator was implanted to allow pacing of the diaphragm during sleep. However, diaphragm pacing was accompanied by paradoxical movement of the rib cage and upper airway occlusion during sleep, and was unsuccessful in maintaining adequate ventilation. Therefore, the patient underwent a tracheostomy after which diaphragm pacing maintained adequate nocturnal ventilation; however, paradoxical movement of the rib cage persisted. The induction of upper airway occlusion as a result of diaphragm pacing, in contrast to the absence of occlusion during spontaneous breathing, highlights the importance of the normal temporal coordination of inspiratory activation of the upper airway muscles and diaphragm. The findings have important implications for the pathogenesis of obstructive sleep apneas in general.
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PMID:Upper airway occlusion induced by diaphragm pacing for primary alveolar hypoventilation: implications for the pathogenesis of obstructive sleep apnea. 697 4

This report describes a young woman with unexplained chronic hypoventilation that was greatly exacerbated during sleep. Treatment with nocturnal O2 during a 2-yr period was associated with stable cardiovascular function but severe morning headaches and lethargy, presumably related to nightly bouts of hypercapnia and acidosis during sleep. A subsequent 2-yr period in which ventilation was assisted during sleep by means of a rocking bed, but supplementary O2 was not used, was associated with disappearance of the headaches and improved psychosocial function, but with the insidious development of signs of pulmonary hypertension and right ventricular hypertrophy. This patient's clinical course demonstrates the separate adverse effects of intermittent hypoxemia and hypercapnia and emphasizes the importance of preventing both hypoxemia and hypercapnia during sleep.
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PMID:Idiopathic hypoventilation syndrome: importance of preventing nocturnal hypoxemia and hypercapnia. 735 98

Persons with sleep apnea syndromes experience 10 or more episodes per hour of sleep during which airflow ceases for more than 10 seconds. Sleep apnea syndromes are classified as obstructive, central or mixed: obstructive when the respiratory muscles continue to contract but airflow is not obtained, central when respiratory effort is not present, and mixed when elements of both obstructive and central apnea are present. Approximately 4 percent of adult men and 2 percent of adult women are believed to have these conditions. In addition to having symptoms such as snoring, headaches, depression, decreased libido and fatigue, patients with sleep apnea are at risk for a range of severe complications secondary to recurrent hypoxia and hypercapnia during sleep. Diagnosis may require an overnight polysomnogram in addition to the history, a physical examination and a laboratory assessment. Less cumbersome diagnostic modalities are being developed. Treatment options include weight reduction, change in sleeping position, avoidance of sedatives, use of continuous positive airway pressure and surgical treatment.
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PMID:Adult sleep apnea syndromes. 765 25

We reported a 39-year-old man with myotonic dystrophy. He suffered from morning headache. Respiratory function tests showed restrictive pattern and arterial gas analysis showed hypoxia and hypercapnia with respiratory acidosis (PaCO2 50.8 mmHg, PaO2 63.8mmHg, pH 7.317, SaO2 89.8%). Polysomnograph showed central apneas exclusively in light sleep (stage 1 and 2). O2 saturation fell at most to as low as 50% during the apneas. We conclude that sleep apnea should be consider in patients with myotonic dystrophy associated with morning headache.
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PMID:[A case of myotonic dystrophy with morning headache following sleep apnea syndrome]. 766 17

A 46-year-old extremely obese black woman presented with headaches, blurred vision, and visual obscurations. Her exam was notable for bilateral severe papilledema, retinal hemorrhages, and lethargy. Her CAT scan was normal, and a spinal tap revealed a very high opening pressure. Although this patient's presentation mimicked pseudotumor cerebri, the lethargy and retinal hemorrhages were atypical. Her hospital evaluation was notable for elevation of the serum bicarbonate level, and she was subsequently found to have hypoxia and hypercapnia on a blood gas. The patient was diagnosed as Pickwickian syndrome, with obstructive sleep apnea. Treatment of the pulmonary problem resulted in dramatic improvement in her eye findings and her lethargy, and optic nerve sheath fenestration was not necessary.
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PMID:Disk edema in an overweight woman. 854 13

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


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