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Query: UMLS:C0018681 (headache)
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After a brief literature survey, the authors share their experience of the treatment of hypertonic crises and acute left cardiac insufficiency of renal patients via Naniprus, a preparation produced in P.R. of Bulgaria. The patients' age was from 11 to 64. With an average basal arterial pressure (AP) 25.2/14.5 kPa during the crises the patients had an average AP of 33.3/20.0 kPa and only three minutes after the initiation of its drop infusion it was reduced to an average of 25. 1/14.7 kPa (p less than 0.001). In one child with severe pulmonary edema in the progress of a hypertonic crisis, in a crisis for rejection of transplanted kidney, they infused Naniprus continuously for 5 days and nights, and in another transplanted patient--7 days and nights, not observing any undesirable effects. The authors recommend Naniprus infusion to be carried out very cautiously, with AP being checked every minute at the beginning at the other side until obtaining the desired and stable result. Each careless or uncontrolled administration of the preparation threatens with severe collapse. In patients with AV-fistulas reddening of the face and eyes as well as headache were observed.
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PMID:[Naniprus treatment of hypertensive crises in patients with kidney diseases]. 716 8

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

Angiotensin converting enzyme inhibitors (ACEI) are established drugs for the treatment of congestive heart failure. Cases of symptomatic hypotension, especially on the first day of treatment, have been reported occasionally. The database we analysed consisted of 1,177 patients, mean age approximately 70 yrs, with congestive heart failure NYHA functional class II or III. These patients were treated and observed prospectively according to a uniform protocol, starting therapy with 2.5 mg enalapril and measuring blood pressure at hourly intervals for eight hours thereafter. 94.6% of the patients experienced no symptomatic hypotension, 4.75% moderate symptoms (e.g. dizziness, headache) and 0.59% severe symptoms (e.g. fainting, collapse, renal failure). For the analyses of risk factors a large number of baseline variables were analysed univariately to select those significant for inclusion in a multivariate stepwise logistic regression. Alternatively the CART-(classification and regression tree) technique was used. Both techniques showed diastolic blood pressure < or = 70 mmHg to be the single most significant risk factor. CART-analyses showed also pretreatment with nitrates and systolic blood pressure < or = 120 mmHg to be of prognostic relevance. Thus CART is a valuable complement when looking for prognostic factors.
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PMID:CART and logistic regression analyses of risk factors for first dose hypotension by an ACE-inhibitor. 814 29

A 23-year-old black female presented with general malaise, headache, high white cell count (136 x 10(9)/L), thrombocytopenia and nephrotic syndrome. She proved to have large granular lymphoproliferative disease with a natural killer cell phenotype and without a clonal rearrangement of the T-cell receptor genes. Renal biopsy demonstrated focal segmental glomerulosclerosis (FSGS). She developed a monophasic neurological illness, and rapidly became comatose six days after the initiation of high dose prednisone therapy. Computerized tomography of the brain showed marked hypodensity of the subcortical white matter. She regained consciousness subsequently, but died six months after her initial presentation with uncontrolled lymphocytosis and renal failure. Autopsy revealed FSGS with glomerular collapse and microcystic dilatation of the renal tubules, and there was perivascular demyelination in the subcortical white matter of the brain. We speculate that lymphokines released by the natural killer cells may have played an important role in the pathogenesis of both the nephrotic syndrome and leukoencephalopathy.
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PMID:Large granular lymphoproliferative disease associated with nephrotic syndrome, renal failure and leukoencephalopathy. 822 Jan 46

Propionitrile, a substituted aliphatic nitrile commonly used in the chemical manufacturing industry, is capable of generating cyanide. However, there are few reports of human intoxication involving propionitrile. We report two workers at an organic chemical manufacturing plant who were overcome by fumes while treating a waste slurry into which unreacted propionitrile was discharged by mistake. One victim was comatose, acidotic, and hypotensive; his blood cyanide level was later measured at 5.0 micrograms/ml. He responded to sodium nitrite/sodium thiosulfate therapy by regaining consciousness. Continued symptoms were treated with hyperbaric oxygen at 2 atmospheres for a total of 4 hours. The second victim, who complained only of nausea, dizziness, and headache and who never lost consciousness, was treated with sodium nitrite/sodium thiosulfate. His measured blood cyanide concentration was 3.5 micrograms/ml. The ambient concentration of propionitrile in air samples at the work site shortly after the exposure was 77.5 mg/m3. In occupational situations in which workers exhibit rapidly progressive symptoms of headache, dizziness, collapse, and coma, and where substituted nitriles are known to be on site, acute cyanide poisoning should be strongly considered. Because of continued endogenous generation of cyanide from the metabolism of the parent compound, hyperbaric oxygen may be a valuable adjunctive therapy to consider, in addition to the immediate use of the cyanide antidote kit, in cases of poisoning by propionitrile or other substituted nitrile compounds. We urge the Occupational Safety and Health Administration to adopt workplace standards for the maximum ambient air concentrations for propionitrile.
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PMID:Successful treatment of life-threatening propionitrile exposure with sodium nitrite/sodium thiosulfate followed by hyperbaric oxygen. 788 67

Quinine poisoning typically results in a constellation of non-life threatening symptoms which include tinnitus, deafness, nausea, vomiting, vision changes, headache, and hypotension. Cardiac conduction defects, dysrhythmias, and cardiovascular collapse have all been reported after overdose and generally occur within 8 hours of ingestion. We report a unique case of delayed cardiotoxicity following quinine ingestion. Toxicity included marked ventricular conduction abnormalities for which serum alkalinization appeared to be therapeutically beneficial, and torsades de pointes requiring overdrive pacing for termination.
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PMID:Delayed cardiotoxicity following quinine overdose: a case report. 834 May 83

Two box jellyfish in particular cause problems in tropical Queensland waters. Chironex fleckeri inhabit calm waters close to the shore between November and May. The venom includes three major components: haemolytic dermatonecrotic and myocardial. The dermatonecrotic toxin causes a ladder pattern of whiplash lesions to the skin which ulcerate become necrotic and heal very slowly over months: Neuromuscular paralysis and cardiovascular collapse may be fatal within minutes of envenomation. Emergency treatment comprises inactivation of stinging capsules by vinegar removal of tentacles analgesia, cardiopulmonary resuscitation and the administration of the specific antivenom. Carukia barnesi ('Irukandji') are found in both coastal and open waters. A patch of erythema with papules at the sting site is characteristically followed 30 min later by the onset of a catecholamine mediated syndrome. Headache and severe abdominal and back pain are usual and may be followed by hypertension, tachyarrhythmias and cardiogenic shock.
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PMID:Marine stingers in far north Queensland. 871 6

Cyanide poisoning presents in many forms. Industrial intoxications occur due to extensive use of cyanide compounds as reaction products. Smoke inhalation, a polyintoxication, is most often responsible for domestic cyanide poisonings. Suicidal poisonings are rare. Cyanogenic compounds may produce acute or subacute toxicity. Signs of cyanide poisoning include headache, vertigo, agitation, confusion, coma, convulsions and death. Definitive laboratory confirmation is generally delayed. Elevated plasma lactate, associated with cardiovascular collapse, should suggest cyanide intoxication. Immediate treatment includes 100% oxygen, assisted ventilation, decontamination, correction of acidosis and blood pressure support. Antidotes include oxygen, hydroxocobalamin, di-cobalt EDTA and methaemoglobin-inducers. Hydroxocobalamin is an attractive antidote due to its rapid cyanide binding and its lack of serious side-effects, even in the absence of cyanide intoxication. Sodium thiosulphate acts more slowly than other antidotes and is indicated in subacute cyanogen poisoning and as an adjunct to acute cyanide poisoning. Initial evaluation of antidotal efficacy is based on correction of hypotension and lactic acidosis; the final analysis rests on the degree of permanent central nervous system injury.
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PMID:Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment. 898 94

Two hundred one consecutive patients with cancer pain who received intrathecal pain treatment between 1985 and 1993 were included in this retrospective study undertaken to test the hypothesis that epidural metastasis is a common cause of "refractory" cancer pain and that its presence may affect the efficacy and the complication rates of intraspinal pain treatment. Fifty-seven (approximately 28%) patients were investigated by metrizamide myelography, computerized tomography (CT), magnetic resonance imaging (MRI), laminectomy, or neurohistopathology. Epidural metastases were found in 40 (70%) and spinal stenosis in 33 (approximately 58%); 7 patients with total and 26 with partial occlusion of the spinal canal. Presence of epidural metastasis affected catheter insertion complications, daily dosages, and complications of the intrathecal pain treatment only when it was associated with spinal canal stenosis (partial or total). During the period of the intrathecal treatment, the patients with confirmed epidural metastasis and total spinal canal stenosis needed significantly (P < 0.05) higher daily doses of opioid (means = 77 +/- 103 versus 22 +/- 29 mg) and intrathecal bupivacaine (means = 65 +/- 44 versus 33 +/- 20 mg) and had significantly (P < 0.05) higher rates (14% versus 0%) of radicular pain at injection and poor distribution of analgesia than those without epidural metastasis and spinal canal stenosis. In contrast, the rate of occurrence of post-dural puncture headache was significantly (P < 0.05) lower in patients with partial (4%) and total (14%) spinal stenosis than in those without (29%). Unexpected paraplegia occurred in four patients and was due to accidental injury during attempted dural puncture (N = 1) and collapse (due to cerebrospinal fluid leakage leading to "medullary coning" of an unknown epidural metastasis (N = 3).
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PMID:Spinal epidural metastasis: implications for spinal analgesia to treat "refractory" cancer pain. 902 59

A 55-year-old obese man was admitted to our hospital because of a severe morning headache. He snored and had recurrent episodes of sleep apnea that began 10 years earlier and had since become much worse. An overnight polysomnographic recording confirmed that he had sleep apnea syndrome, predominantly of the central type. The apneas were more frequent when he lay on his back (apnea index 54.5) than on his side (apnea index 1.2). He was treated with sleep position adjustment and nasal bi-level positive airway pressure, inspiratory positive airway pressure at 5 cmH2O and expiratory positive airway pressure at 2 cmH2O. His snoring, headache, and oxygen desaturation resolved. This case suggests that airway collapse may cause central apnea, and that nasal continuous positive airway pressure, and nasal bi-level positive airway pressure and adjustment of sleep position can be effective in some patients with central-type sleep apnea syndrome.
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PMID:[Central sleep apnea syndrome successfully treated with nasal bi-level positive airway pressure and sleep position adjustment]. 916 57


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