Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The side-effects of two opioid agonist-antagonists, nalbuphine and pentazocine, were assessed when used for patient-controlled postoperative analgesia. Forty ASA I or II patients scheduled for upper abdominal surgery were randomly allocated to two equal groups. The anaesthetic technique was the same for all the patients: premedication with atropine and diazepam, induction with thiopentone and suxamethonium and maintenance with fentanyl, pancuronium, nitrous oxide and halothane. Patient-controlled computer assisted analgesia (On-Demand Analgesia Computer) was started in the recovery room at least 2 h after the last administration of fentanyl. The parameters used were: a routine hourly dose (the half of that received during the previous hour), with on demand delivery of nalbuphine (15 micrograms.kg-1) or pentazocine (45 micrograms.kg-1) aliquots respectively, with a refractory period between two demands of 4 min and a total hourly maximum dose of 16 mg and 48 mg respectively. The following parameters were measured before the start of self-administration, and every hour afterwards for 24 h: systolic (Pasys) and diastolic blood pressures, heart rate, pressure-rate product (PRP), respiratory rate, end-tidal CO2 and pain (by way of a three point scale). Analgesia was assessed on a four-point scale every 6 h. The total doses of nalbuphine and pentazocine administered were 94 +/- 43 mg and 251 +/- 150 mg respectively. The only parameters significantly different between the two groups were Pasys and PRP, being higher in the pentazocine group. There were no significant differences in the side-effects (drowsiness, nausea, vomiting, headache, amnesia, logorrhoea and urine retention). All patients in both groups were satisfied with this technique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of nalbuphine and pentazocine in the treatment of postoperative pain by self-administration]. 266 Jun 40

A case of an acute intracranial subdural haematoma occurring shortly after spinal anaesthesia is reported. A 67 year old poorly controlled hypertensive man, ASA II, underwent removal of a prostatic adenoma under spinal anaesthesia. He complained of postural headache on the third day after surgery. Unresponsive to the usual analgesics, his headache became severe, persistent and non postural on the fifth day. Twenty-four hours later, he suddenly presented with a left hemiplegia and became comatose. Computed axial tomography showed a large left-sided subdural haematoma, lying over the left hemisphere. During the immediate surgical removal, a pulsatile arterial bleeding originating from a small cortical artery was discovered, and stopped. The patient slowly recovered consciousness, but the hemiplegia remained. He finally died six months later of bronchopneumonia. The link between the haematoma and the spinal anaesthetic is not proven; the possible relationship between the two is discussed.
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PMID:[Acute intracranial subdural hematoma of arterial origin after spinal anesthesia]. 273 74

In order to study the role of platelets in migraine and cerebrovascular disease, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) plasma levels, indices of in vivo platelet activation, were assayed in two groups of patients suffering from migraine (common/classic and classic/complicated migraine, respectively) and in one group suffering from transitory ischemic attacks (TIAs). Plasma determinations were carried out in the absence of treatment and during the administration of aspirin (50 mg/daily) and flunarizine (10 mg/daily). Platelet activation was found in patients suffering from TIA; patients affected by classic and complicated migraine showed a high incidence of activation, in comparison with common migraine sufferers, also in headache-free periods. Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs. Aspirin, however, did not affect platelet activation in subjects suffering from ischemic attack even though we did not observe any relapse after one year of treatment. The different effect of ASA in TIAs and migraine indicates that the platelet activation in TIA patients is due not only to cyclo-oxygenase pathway but also to other in vivo pathways.
Cephalalgia 1985 May
PMID:Drugs and platelet activation in migraine and transient ischemic attacks. 316 Apr 72

The efficacy of the combination of dihydroergotamine (10 mg) with acetylsalicylic acid (80 mg) (DHE + ASA) in the prophylaxis of migraine was studied in a double-blind, placebo-controlled crossover trial (8 weeks twice). Of 45 patients who entered the study, 38 completed it. The number of attacks was significantly (p = 0.003) reduced during active treatment (11.5 +/- 6.2) compared with placebo (16.6 +/- 9.9). The mean duration, the mean severity, and the mean score for symptomatic acute medication of attacks did not differ significantly. The overall assessment made by the patients themselves was in favor of DHE + ASA (p = 0.001). These results indicate a moderately beneficial effect of the dihydroergotamine/low-dose acetylsalicylic acid combination in migraine prophylaxis.
Cephalalgia 1988 Sep
PMID:Combined low-dose acetylsalicylic acid and dihydroergotamine in migraine prophylaxis. A double-blind, placebo-controlled crossover study. 319 98

Plasma aspirin and salicylate concentrations were followed after 600 mg of a new palatable glycinated preparation of aspirin was given to six healthy male volunteers in an attempt to investigate whether pre-gastric absorption of aspirin could occur. In each subject the drug was administered by three different routes, viz. (i) swallowed with water, (ii) dissolved sublingually and retained in the mouth, and (iii) allowed to disperse on the tongue, and then swallowed without water intake. Using the latter route of administration and the same aspirin formulation, plasma aspirin and salicylate concentrations were also followed in 10 patients during acute migraine attacks. These results were compared with those from another 10 migraineurs given 600 mg of soluble aspirin swallowed with water during attacks. Aspirin and salicylate pharmacokinetic parameters (Cmax, tmax, t1/2, Kabs and AUC) in the normal volunteers were not significantly different (p greater than 0.05) whether glycinated aspirin was swallowed with water or swallowed without water after dispersion in the mouth. However, negligible aspirin was absorbed when the glycinated preparation was retained in the mouth. In migraine patients, there was no significant difference (p greater than 0.05) between the bioavailabilities of soluble aspirin swallowed with water (AUC = 5.7 +/- 2.3 mg h/l) and glycinated aspirin swallowed without water (AUC = 4.4 +/- 1.6 mg h/l). There also was no significant difference (p greater than 0.05) when the time courses of pain relief were compared, both treatments being associated with a significant (p less than 0.01) analgesic effect. The glycinated aspirin was thus bioequivalent to swallowed aspirin but has no advantages for migraineurs over soluble aspirin if water is readily available for self-administration.
Cephalalgia 1986 Mar
PMID:A new formulation of aspirin: bioavailability and analgesic efficacy in migraine attacks. 351 7

The currently recognized toxic effects of quinine in humans are identified and the problems of management of overdosage of quinine are discussed. Quinine, available therapeutically as sulphate or hydrochloride salts, also is widely used in tonic water, and there are several case reports of allergic reactions to the drug when a patient has consumed the drug in this way. Another unintentional source of poisoning is its use as an adulterant in heroin for "street" use. This appears to be a problem in the US. Quinine, termed a "general protoplasmic poison" is toxic to many bacteria, yeasts, and trypanosomes, as well as to malarial plasmodia. Quinine has local anesthetic action but also is an irritant. The irritant effects may be responsible in part for the nausea associated with its clinical use. In addition it has a mild antipyretic effect. Several features are common to both an acute single overdose in self-poisoning and accumulation of quinine during therapy for malaria: together they are termed cinchonism. Auditory symptoms, gastrointestinal disturbances, vasodilatation, sweating, and headache occur with moderately elevated plasma quinine concentration. As these rise, increasingly severe visual disturbances and then cardiac and neurologic features occur. Mild nausea may be the only symptom, but with large overdoses profuse vomiting, abdominal pain, and diarrhea may occur. These result from a combination of the local irritant effect of quinine on the gut and the central effects of quinine on the chemoreceptor trigger zone. Vasodilatation and sweating are well recognized, and tinnitus is common. Visual symptoms usually are delayed, and blindness may not be discovered for a day or more. Aspirin-sensitive patients, and others, may develop angioedema by nonimmunological mechanisms in response to drugs, and quinine has been reported to produce pseudo-allergic reactions in aspirin-sensitive patients. Quinine also can cause drug-induced thrombocytopenia and purpura. In patients suffering with malaria due to "Plasmodium falciparum," anemia and acute intravascular hemolysis with renal failure are recognized complications. There appears to be little evidence in the literature in support of the folk tradition of quinine as an inducer of abortion. Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. Clinically, quinine poisoning is observed in 3 situations: self-poisoning; accidentally; and following use of quinine in excessive doses in the hope of achieving abortion. Treatment courses are reviewed.
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PMID:Quinine toxicity. 354 70

The anesthetic effect of 2 ml of 5% lidocaine in 7.5% glucose (LG) or 5% meperidine in water were evaluated and compared in 40 ASA class 1 or 2 patients. Patients were randomly assigned to one of the two groups (20 patients in each) according to the anesthetic agent, which was injected into the lumbar subarachnoid space in the sitting position. The patients remained sitting for 5 min before being placed in the supine position. Times of onset of sensory and complete motor blockade were significantly more rapid with LG. The extent of maximum cephalad spread of analgesia and the time to maximum height of analgesia in the two groups were not different. Duration of analgesia at the T-7 (48.96 +/- 6.64 min with LG, 44.74 +/- 6.14 min with meperidine; means +/- SEM) and L-1 (94.37 +/- 7.42 min with LG, 76.19 +/- 5.64 min with meperidine) dermatomes was not different in the two groups but was statistically longer at the T-10 dermatome with LG (66.83 +/- 6.72 min) than with meperidine (46.66 +/- 6.26 min). The duration of complete motor blockade was also significantly longer with LG (66.44 +/- 7.05 min) than with meperidine (42.67 +/- 4.47 min). Complications in both groups included decrease in blood pressure and nausea and vomiting intraoperatively, and urinary retention, nausea and vomiting, and mild headache postoperatively. Complications that occurred only in the meperidine group were intraoperative drowsiness, respiratory depression, bronchospasm, and itching. The frequency of complications was greater wit meperidine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Meperidine as a spinal anesthetic agent: a comparison with lidocaine-glucose. 354 85

Nine children, aged 5 to 11 years, with subacute or chronic meningitis were studied. Symptoms started during the summer season in all patients and in eight of the patients the disease began with a localized erythematous lesion (ECM), mostly in the face. In one patient only there was a history of an insect bite at the site of the erythema. The neurological abnormalities included aseptic meningitis, peripheral facial nerve palsy (5/9) and oculomotor nerve palsy (1/9). Most children complained of headache, fatigue, loss of appetite and had a low grade fever. High antibody titers to Borrelia spirochetes in serum and/or cerebrospinal fluid (CSF) were demonstrated by ELISA in eight of the nine patients and by indirect immunofluorescence assay (IFA) in three patients. All patients had a dramatic improvement in their general condition and became afebrile within three days of institution of i.v. penicillin G treatment (i.v. cefuroxime in one patient).
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PMID:Tick-borne Borrelia-meningitis in children. An outbreak in the Kalmar area during the summer of 1984. 359 Dec 90

The effect of daily aspirin (ASA) administration after "desensitisation" was studied in 16 aspirin-sensitive asthmatics. Fourteen patients completed the trial; 12 of them also had perennial rhinitis and eight in addition suffered from chronic headache. During 4 weeks of daily treatment with 600 mg of ASA a marked reduction of the nasal symptoms score was noticed in 8/12 patients and head pain score was significantly decreased in 6/8 patients when compared with the 4-week non-ASA period. Daily aspirin resulted in decreases in both the mean asthma score and in daily beta-agonist usage in 7/14 patients, and 10/13 patients showed a decrease in bronchial responsiveness to inhaled histamine (geometric mean of provocative concentration of histamine 1.8 and 5.8 mg/ml, respectively. In four patients we noticed untoward epigastric symptoms. A decrease in thrombocyte counts was observed during ASA treatment. Our study suggests that daily aspirin administration after "desensitisation" may be helpful in the management of some ASA-sensitive asthmatics.
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PMID:Clinical efficacy of aspirin in "desensitised" aspirin-sensitive asthmatics. 381 57

Aspirin 650 mg and metoclopramide 10 mg in an effervescent preparation (Migravess) were compared with effervescent aspirin 650 mg (Alka-Seltzer) and placebo for common migraine attacks with a double-blind cross-over design. One hundred and eighteen patients with common migraine were entered. Eighty-five patients completed all three forms of treatment, eleven completed two, and six completed one. Medicine was taken when patients were sure they had a migraine attack and not just interval headache. After each form of treatment, they mailed a report form to the investigators. Additional medication was allowed after 2 h and was taken for 79/95 placebo treated attacks, 63/92 Migravess treated attacks, and 51/86 aspirin treated attacks (p less than 0.01). Aspirin was significantly better than placebo for pain but not quite significant for nausea. Migravess was significantly better than placebo for pain and for nausea. There was no significant difference between aspirin and Migravess with regard to analgesic effectiveness (p = 0.33) or to antinausea effect (p = 0.18).
Cephalalgia 1984 Jun
PMID:Effervescent metoclopramide and aspirin (Migravess) versus effervescent aspirin or placebo for migraine attacks: a double-blind study. 637 73


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