Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspirin and acetaminophen have excellent and essentially similar antipyretic activity. For the child, lowering of temperature will be indicated for excessively high temperature and when there is a history of febrile seizures. Specific clinical contraindications will often dictate the selection of one drug over the other. Aspirin has some advantage over acetaminophen for analgesia. The need for either drug for analgesia in the pediatric patient, however, will be infrequent; when required, a drug with greater analgesic activity than either aspirin or acetaminophen may be indicated.
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PMID:Aspirin and acetaminophen: a comparative view of their antipyretic and analgesic activity. 36

General principles of thermoregulation, the pathophysiology of fever, controversies concerning the use of antipyretic therapy, and nonpharmacologic and pharmacologic treatments commonly used for antipyresis in the pediatric population are reviewed. Several arguments can be made for not ameliorating the febrile response. Fever is an important diagnostic and prognostic clinical sign that may have beneficial effects for the host. In addition, body temperatures of < or = 41 degrees C (105.8 degrees F) are relatively harmless. Reasons for treating fever include patient discomfort, the potential for adverse sequelae, the possibility of seizures, and the possibility that fever could affect the pharmacokinetic profiles of drugs. Nonpharmacologic treatment for fever includes environmental measures to enhance dissipation of body heat and sponging. Aspirin and acetaminophen are the agents used most frequently for antipyresis in pediatric patients. However, aspirin use in children with a viral illness has been associated with development of Reye's syndrome. As a result, its use in children has declined in the United States. Acetaminophen is relatively free of adverse effects and is considered first-line pharmacologic antipyresis therapy. Ibuprofen suspension should be considered as second-line antipyretic therapy. Combination therapy with acetaminophen and aspirin may be considered if the patient fails to respond to other nonpharmacologic and pharmacologic therapies; however, combination therapy may result in increased risk of drug toxicity, increased probability of adverse reactions, and increased risk of intoxication. Aspirin, acetaminophen, and ibuprofen are equally effective for antipyresis in pediatric patients. However, because acetaminophen is the safest medication, it is currently the therapy of choice.
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PMID:Antipyretic therapy in the febrile child. 128 50

We evaluated the clinical effectiveness of esmolol, an ultra-short-acting, beta-adrenergic receptor blocking drug, to control the sinus tachycardia and increase in arterial blood pressure induced by electroconvulsive therapy (ECT). Each of 20 patients, ASA physical status I-III, participated in a double-blind, randomized Latin-Square study involving two matched-pair trials (placebo versus esmolol given as a 500-micrograms/kg bolus followed by either 300 micrograms.kg-1.min-1 [high dose], 200 micrograms.kg-1.min-1 [medium dose], or 100 micrograms.kg-1.min-1 [low dose] infusion of esmolol) during ECT. Each patient acted as his or her own control (total number of ECT procedures were 160). We administered a 1-min bolus of placebo (normal saline) or esmolol at the rate of 500 micrograms.kg-1.min-1 followed by either high-, medium-, or low-dose esmolol or placebo for an additional 3 min. We then induced anesthesia with methohexital (1 mg/kg) and succinylcholine (0.5 mg/kg) IV. Ninety seconds after the administration of succinylcholine, the electrical stimulus was applied to induce seizure. The infusion of placebo or esmolol was discontinued 3 min after the electrical stimulus. Significant decreases were found in mean heart rate from minute 3 until minute 7 and in the maximum heart rate. The mean of each patient's maximum heart rate after seizure changed from 147 +/- 18 bpm in placebo patients to 112 +/- 20 bpm in high-dose esmolol patients; to 121 +/- 23 bpm in medium-dose esmolol patients; and to 124 +/- 20 bpm in low-dose esmolol patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Defining the dose range for esmolol used in electroconvulsive therapy hemodynamic attenuation. 135 3

The clinical features of 19 patients with neurological manifestations unexplained by another disease and positive serology for Borrelia burgdorferi were studied. ECM was present in only 11% of the cases and 32% referred tick bite. The characteristic features for suspicion of NB according to our series was the presence of polyneuritis in 84% of the cases specially in the form of multiple mononeuritis and involvement of the facial nerve (79%) leading to even greater suspicion with the association of V pair involvement. Seizures, sleep disorders, and higher mental dysfunction may be found in association with other more characteristic neurological features. The typical triad of NB (aseptic meningitis, facial paralysis and polyradiculoneuritis) was found in 21% of the patients and in the absence of another disease to justify the same neuroborreliosis (NB) seemed evident. In all the cases components of this triad were found. Headache, arthralgia, fever and, less frequently, arthritis are other symptoms often past with the presence of anti-BB antibodies. Patients with the shortest evolution most frequently presented antecedents of facial paralysis, sensory alterations and Romberg's sign than patients of longer evolution. CSF demonstrated the presence of pleocytosis in 24% of the cases and in only one patient a slight increase in the intrathecal activity of IgG was observed which may be of use in differential diagnosis with MS. MR showed alterations in 61% of the patients and, while not specific, the lesions present subcortical predominance.
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PMID:[Positive anti-Borrelia antibodies in patients with clinical manifestations compatible with neuroborreliosis]. 161 Jun

Twelve ASA physical status I-III patients were enrolled in a double-blind, prospective, randomized, three-way, within-patient crossover study designed to determine the effect of two standard esmolol bolus doses (100 and 200 mg) on the haemodynamic response and seizure duration during electro-convulsive therapy (ECT). Esmolol or placebo was administered one minute prior to induction of anaesthesia and exactly two minutes before ECT. Both the 100 and 200 mg bolus doses significantly blunted the maximum increase in heart rate (HR) and mean arterial pressure (MAP) following ECT in comparison with placebo. Compared with placebo, esmolol 100 mg decreased maximum HR by 23 +/- 3%, maximum MAP by 17 +/- 7% and maximum rate-pressure product (RPP) by 40 +/- 9%. Esmolol 200 mg decreased maximum HR by 25 +/- 3%, maximum MAP by 19 +/- 3% and maximum RPP by 42 +/- 5%. No significant difference was found between the two esmolol doses at corresponding measurement points before and after ECT. Treatment with esmolol 200 mg resulted in a significantly shorter mean seizure duration than with placebo. As the 200 mg dose caused a shorter seizure duration and the haemodynamic effects of 100 mg and 200 mg doses were similar, it was concluded that the 100 mg esmolol bolus dose was the better dose for ECT.
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PMID:Comparison of two esmolol bolus doses on the haemodynamic response and seizure duration during electroconvulsive therapy. 167 42

To determine whether a standardized dose of esmolol can effectively attenuate the cardiovascular response to electroconvulsive therapy (ECT), 17 ASA physical status I-II patients were studied in a randomized within-patient, crossover design. Each patient received "no esmolol" during one ECT and three to five days later crossed over to the alternative treatment receiving an esmolol 80 mg bolus followed by 24 mg.min-1 infusion two minutes prior to induction of anaesthesia and continued for five minutes after induction. Esmolol blunted the maximum increases in heart rate (HR) by 26 per cent, mean arterial pressure (MAP) by 14 per cent, and rate pressure product by 37 per cent with significant differences (P less than 0.05) noted at one, two, three and four minutes after ECT (minutes five, six, seven, and eight of the esmolol infusion). There was no significant difference in seizure duration between the two groups and no adverse reactions occurred.
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PMID:Esmolol bolus and infusion attenuates increases in blood pressure and heart rate during electroconvulsive therapy. 196 27

We evaluated the clinical effectiveness of esmolol, an ultra-short-acting beta 1-adrenergic receptor blocking drug, to control the sinus tachycardia and increase in arterial blood pressures induced by electroconvulsive therapy (ECT). Each of 20 patients, ASA physical status I-III, participated in a double-blind, randomized study, involving four match-pair trials (placebo versus esmolol) during ECT. Each patient acted as his or her own control (total number of ECT procedures, 160). We administered a 4-min infusion of either placebo or esmolol at the rate of 500 micrograms.kg-1.min-1. We then induced anesthesia with methohexital and succinylcholine. After administration of electrical stimulation for ECT, the rate of infusion decreased to 300 micrograms.kg-1.min-1 for three additional minutes and was then discontinued. Statistically significant reductions in mean heart rate from minute 2 until minute 15 and in maximum heart rate (the mean of each patient's maximum heart rate after seizure changed from 152 +/- 23 to 115 +/- 24 beats/min) occurred in patients given esmolol. During and immediately after infusion, arterial blood pressure also decreased. Finally, the length of seizures decreased, as manifested clinically from 48 +/- 18 to 39 +/- 14 s and on electroencephalogram from 86 +/- 41 to 67 +/- 28 s. We conclude that esmolol effectively controls the hyperdynamic response to ECT and reduces the length of seizures. The significance of the latter to the overall effectiveness of ECT is not known.
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PMID:Esmolol reduces autonomic hypersensitivity and length of seizures induced by electroconvulsive therapy. 197 95

Two young patients (a brother and his sister) with low ASA levels who had myoclonic seizures since the age of eight years, were investigated by means of electrophysiological, neuroradiological and laboratory tests and submitted to a physical examination. In both patients, the disease started at the age of eight years with drug resistent myoclonic seizures. Intelligence was not impaired and ASA levels were lower than normal, but clinical features were not those of classic MLD. Electrophysiological study revealed altered SEPs and normal BAEPs (they are both altered in leukodystrophy). Therefore our findings conclude that tour patients must be considered "Neurological patients non-MLD with low levels of ASA".
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PMID:On a rare atypical form of metachromatic leukodystrophy (MLD): "neurological non-mld patients with low levels of arylsulphatase A". Description of two cases. 257 49

The case of a 4 years old boy, hospitalized for an unexplained coma, is reported. He is the first child of a non-consanguin couple. The psychomotor development of this child was considered as normal up to the age of 18 months; then, a delay in language development, behaviour disorders with an important instability interrupted by episodes of somnolence, were observed. This child was treated for psychotic disorders. At the age of 3 and half, he had two episodes of seizures associated with fever. He was hospitalized for a 24 hours coma (4 years old). An hepatomegaly and a dry, brittle hair were then observed. Hyperammonemia was made obvious by a protein tolerance test. The diagnosis of argininosuccinate lyase (ASAL) deficiency was based on the increased levels of ASA in plasma and urine. The deficiency was proved by a fibroblast culture. With protein restriction, hepatomegaly disappeared, hair became normal, the behaviour disorders and the delay in language development was improved. However, some school difficulties persist. This case shows that an hereditary metabolic syndrome can be revealed by psychotic like symptoms in childhood.
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PMID:[Argininosuccinic aciduria. A new case revealed by psychiatric disorders]. 271 82

Administration of convulsant doses of pentetrazole induced an increase of PGF2 alpha, PGE2 and TXB2 immuno-reactive material in mouse brain in vivo. The non-steroidal anti-inflammatory drugs indomethacin, flurbiprofen and diclofenac in equipotent doses inhibited the convulsion-induced increase of prostaglandins and thromboxane B2 (P less than 0.01). The same drugs also lowered the LD50 of pentetrazole (P less than 0.05) and accelerated the onset of tonic seizures evoked by pentetrazole (P less than 0.05). Ibuprofen in a submaximal centrally effective dose acted in the same way on cerebral PG and TXB2 synthesis and on the LD50 of pentetrazole but failed to influence significantly the latency time to the onset of pentetrazole-induced tonic seizures. Aspirin (100 mg/kg) and paracetamol (30 mg/kg), which were without effect on cerebral PG and TXB2 concentrations following pentetrazole-induced seizures, were also ineffective in lowering the convulsive threshold and the LD50 of pentetrazole. It is concluded that non-steroidal anti-inflammatory drugs act on the convulsive threshold by inhibition of cerebral prostaglandin and/or thromboxane synthesis.
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PMID:Lowering of the convulsive threshold by non-steroidal anti-inflammatory drugs. 720 18


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