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

Hypocalcemia, although a relatively uncommon sequela of operations for carcinoma of the larynx and pharynx, often presents as an acute medical emergency. In its chronic form, hypocalcemia may be a difficult disorder to control. Understanding the etiologic basis of hypocalcemia secondary to operations for carcinoma of the head and neck requires knowledge of the pathophysiology of the preoperative and postoperative factors affecting calcium homeostasis. These factors include thyroidectomy, hypoparathyroidism, hypomagnesemia, anticonvulsant therapy, estrogen replacement therapy, oral contraceptives, blood transfusions, hyperventilation alkalosis, hypoalbuminemia, corticosteroid therapy, depression, emotional stress and diet. Often the onset of symptoms and signs of hypocalcemia occurs within 24 to 48 hours after the operation. The symptoms may include mental depression, headache, tingling of the hands and perioral region and abdominal pain. Unrecognized chronic hypocalcemia may lead to the development of cataracts, convulsions and psychosis.
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PMID:Etiologic factors in hypocalcemia secondary to operations for carcinoma of the pharynx and larynx. 67 61

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

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Headaches may occur in as many as 25% of hypertensive patients and generally bears little relationship to level of diastolic blood pressure. Previous observations, in normotensive patients, suggested that abnormalities in both potassium and ammonia metabolism might be related to the pathogenesis of these headaches. The present study was undertaken to see whether these factors also occurred in hypertensive patients with headaches. The present observations were made in thirteen hypertensive patients with vascular headaches. The major findings include potassium levels of 3.45 +/- 0.25 mEq/L; CO2, 29.85 +/- 1.21 mEq/L; blood ammonia, 41 +/- 8.40 U mol/L and an alkaline pH of the urine. The blood ammonia levels, when factored by the BUN, yielded elevated ammonia to BUN ratios (3.81 +/- 1.82). These findings are similar to those previously observed in normotensive patients with vascular headaches. The profile of hypokalemia and/or alkalosis, increased blood ammonia to BUN ratios and a relatively alkaline urine appears to be a commonly observed pattern in patients with vascular headaches. These data suggest that a biochemical basis exists for the genesis of vascular headaches in patients with hypertension.
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PMID:The pathogenesis of vascular headaches in patients with hypertension; the role of the ammonia-potassium axis. 364 6

A conceptual approach that relates vascular headaches, bowel and bladder dysfunction to abnormalities of the "ammonia potassium axis" is presented. Hypokalemia alters smooth muscle function of both the bowel and bladder and results in the elaboration of an alkaline urine. The occurrence of an alkaline urine, along with bladder dysfunction and urinary stasis, predisposes to recurrent urinary tract infections. Hypokalemia and/or alkalosis increases the renal return of ammonia, exposes the brain to chronically higher concentration of ammonia and facilitates its passage into the central nervous system. Increased levels of blood ammonia predispose to hyperventilation which results in a superimposed respiratory alkalosis on a pre-existing hypokalemia and/or alkalosis therefore causing intense cerebral vasoconstriction. Varying degrees of cerebral ischemia and hypoxia occur and give rise to higher brain concentrations of ammonia. Vasodilatation occurs during the headache phase and may be a consequence of the sudden increase of brain ammonia and/or due to the release of other vasoactive mediators. As a consequence of increased blood ammonia, a reduction of protein intake may result in the alterations of amino acid precursors for brain uptake and therefore further interferes with the modulation of cerebral blood flow and brain function.
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PMID:The hypokalemic, bowel, bladder, headache relationship; a new syndrome. The role of the potassium ammonia axis. 651 31

We investigated an outbreak of illness in electronics plant workers. Questionnaire data revealed that 98 employees experienced symptoms, including light- headedness , headache, sleepiness, and numbness/tingling of the face or extremities. Attack rates by work station followed no apparent pattern. Extensive medical and environmental evaluation, including air sampling for numerous solvents and gases, provided no physical or chemical explanation for the epidemic. Compared with well employees, ill employees were more commonly female, complained more frequently of bothersome odors, and believed that greater danger existed of the illness recurring. Blood gas analyses of seven of 11 ill workers showed respiratory alkalosis, consistent with hyperventilation. The poorly defined nature of this illness, the absence of exposures to environmental contaminants in concentrations exceeding recommended limits, and the evidence of hyperventilation suggest that this outbreak was an incident of industrial psychogenic illness.
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PMID:An epidemic of psychogenic illness in an electronics plant. 672 87

A 29-year-old male climber developed high altitude pulmonary edema (HAPE), progressing from headache and dyspnea to disturbance of consciousness in the Japan Alps. He was admitted to Shinshu University Hospital. Physical examination on admission revealed a cyanotic patient with coarse crackles and wheezes in bilateral lungs. Chest X-ray film showed bilateral patchy infiltrates. Arterial blood gases indicated severe hypoxemia, and respiratory alkalosis; pH 7.452, PO2 35.5 Torr, PCO2 31.6 Torr. Right heart catheterization showed noncardiogenic pulmonary edema, analysis of bronchoalveolar lavage (BAL) fluid was as follows; cells 2.05 x 10(5)/ml (alveolar macrophages 61.5%, neutrophils 25.5%, lymphocytes 13.0%), protein concentration 91 mg/dl. Cellular and protein analysis of BAL has been shown to be of value to clarify the pathogenesis of the permeability edema in patients with HAPE.
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PMID:[Analysis of bronchoalveolar lavage fluid in a case of high altitude pulmonary edema]. 834 13

We report the case of a 33-year-old man who presented with headaches and vomiting. Soon after admission he became drowsy and agitated, developed ventricular tachycardia and his neurological state worsened (Glasgow coma score 6). Blood analysis showed respiratory alkalosis, hyperlactacidemia (8 mmol/l), hyperammonemia (390 micro mol/l) and hypoglycaemia (2.4 mmol/l). Subsequently, he developed supraventricular tachycardia, ventricular tachycardia and ultimately ventricular fibrillation resulting in cardiac arrest, which was successfully treated. A CT scan of the head revealed cerebral oedema. Whilst in the intensive care unit, he developed renal failure and rhabdomyolysis. The metabolic abnormalities seen at the time of admission normalised within 48 h with IV glucose infusion. Biological investigations, including urinary organic acids and plasma acylcarnitines, showed results compatible with MCAD deficiency. Mutation analysis revealed the patient was homozygous for the classical mutation A985G. This is one of only a few reports of severe cardiac arrhythmia in an adult due to MCAD deficiency. This condition is probably under-diagnosed in adult patients with acute neurological and/or cardiac presentations.
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PMID:Adult presentation of MCAD deficiency revealed by coma and severe arrythmias. 1289 89

Reversible cerebral vasoconstriction syndrome (RCVS) has reversible multifocal narrowing of the cerebral arteries. Respiratory alkalosis in high altitude studies cause impairment of the central nervous system, presumably by cerebral vasoconstriction. A 54 year-old woman presented with a 1-week of throbbing headache around her forehead while travelling in moderately high altitude, during a windy winter. Sudden severe headache had progressed and developed bilateral lower visual fields defect along with mild weakness of her right leg on the next day. Magnetic resonance (MR) imaging revealed acute ischemic process at both occipital, parasagittal left parietal and right frontal area. MR venography was negative but MR angiography showed multifocal narrowing of both anterior and posterior circulations. Lumbar puncture revealed the opening pressure of 240 mmH2O but normal CSF profiles. Blood tests, including complete blood count, protein C, protein S, antithrombin III, high-sensitivity C-reactive protein, immunologic and antibody profiles were normal. Dexamethasone and low-molecular weight heparin were given because the intracranial vasculitis and cerebral venous thrombosis could not be ruled out. Visual fields and right leg problems had fully recovered on the second day and second week respectively. Prednisolone was discontinued at the fourth week. MR imaging and MR angiography were repeated in the sixteenth week and revealed old infarction at the left posterior parietal area but narrowing segment of arterial systems were no longer seen. There were a few previous reported cases of RCVS in Asian counties. The authors proposed that altitude changes from travelling to the moderately high altitude and cold windy winter weather were the predisposing factors for the attack of RCVS.
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PMID:Reversible cerebral vasoconstriction syndrome with increased intracranial pressure, probably related to altitude changes and windy winter travelling. 2167 54

An 18-year-old woman with Gitelman syndrome (GS) associated with idiopathic intracranial hypertension (IIH) is described. She was obese and showed a 10 kg gain in body weight over a period of 8 months. She presented with headache, vomiting, and diplopia. She had bilateral papilledema, and right abducens palsy. CSF examination demonstrated high pressure (over 320 mmH(2)O) with normal cytochemistry. Brain MRI was normal. She showed mild alkalosis, hypokalemia, hypomagnesemia, increased plasma renin activity, and normal blood pressure. Two heterozygous mutations in the SLC12A3 gene were identified. Therefore, she was diagnosed as GS with IIH. We should keep in mind the possible occurrence of IIH in GS.
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PMID:A case of Gitelman syndrome associated with idiopathic intracranial hypertension. 2175 36


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