Disease relevance of Ativan

• A comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus [1].
• We conducted a five-year randomized, double-blind, multicenter trial of four intravenous regimens: diazepam (0.15 mg per kilogram of body weight) followed by phenytoin (18 mg per kilogram), lorazepam (0.1 mg per kilogram), phenobarbital (15 mg per kilogram), and phenytoin (18 mg per kilogram) [2].
• Adults with prolonged (lasting five minutes or more) or repetitive generalized convulsive seizures received intravenous diazepam (5 mg), lorazepam (2 mg), or placebo [1].
• Lorazepam in myoclonic seizures after cardiac arrest [3].
• The intense sleepiness induced by lorazepam in some of the abusers, despite their significantly lower plasma concentrations, should alert clinicians of the potential toxicity from accentuated responses to sedative hypnotics in active cocaine-abusing subjects [4].

Psychiatry related information on Ativan

• Failure of buspirone to protect against lorazepam withdrawal symptoms [5].
• Measures of family attitudes (expressed emotion [EE]) and interactional behaviors (affective style [AS]), both of which have been found to predict relapse in schizophrenia, were obtained from key relatives of 23 hospitalized recently manic bipolar patients [6].
• OBJECTIVE: To determine if the APOE epsilon4 allele increases susceptibility to lorazepam-induced verbal learning impairment in nondemented older adults [7].
• Significant differences also emerged on the Brief Psychiatric Rating Scale and in the number of supplemental doses of lorazepam required by the patients in each group [8].
• Task-related neural activity in bilateral PFC showed a predicted pattern: an Emotion x Stimulus crossover interaction, with no main effects, with activity predicting task performance [9].

High impact information on Ativan

• After adjustment for covariates, the odds ratio for termination of status epilepticus by the time of arrival in the lorazepam group as compared with the placebo group was 4.8 (95 percent confidence interval, 1.9 to 13.0) [1].
• Genomic imprinting. Silence across the border [10].
• Human genetics. Silence speaks in spectrin [11].
• Apolipoprotein E epsilon4 allele and lorazepam effects on memory in high-functioning older adults [7].
• Dose-dependent decrease of activation in bilateral amygdala and insula by lorazepam during emotion processing [12].

Chemical compound and disease context of Ativan

• CONCLUSIONS: As initial intravenous treatment for overt generalized convulsive status epilepticus, lorazepam is more effective than phenytoin [2].
• MAIN OUTCOME MEASURE: We used the Buschke Selective Reminding Test to assess verbal learning during a 5-hour period after placebo or lorazepam administration [7].
• BACKGROUND: An increasing number of case reports indicate a superior therapeutic response of catatonialike symptoms, such as severe psychomotor disturbance and mutism, associated with psychiatric disorder to the benzodiazepine lorazepam (LO) [13].
• We administered a "cocktail" of three model substrates for hepatic processes: antipyrine for oxidation, lorazepam for glucuronidation, and indocyanine green for hepatic blood flow, to children with acute lymphocytic leukemia (ALL) [14].
• In a double-blind, randomized, crossover study, 58 patients with postherpetic neuralgia received 6-week courses of amitriptyline, 12.5 to 150 mg/d; lorazepam, 0.5 to 6 mg/d; or lactose placebo [15].

Biological context of Ativan

• Very small concentrations of IIc displaced [3H]diazepam completely from specific cerebral receptors, but not from liver and kidney binding sites; the concentration causing 50% inhibition of specific [3H]diazepam binding (IC50) was 4-7 nM compared to ca. 5 nM for the potent benzodiazepine lorazepam [16].
• Clinical pharmacokinetics of lorazepam. I. Absorption and disposition of oral 14C-lorazepam [17].
• Thus, the aging process is associated with small changes in the kinetics of lorazepam [18].
• Peak visually guided saccade velocity was decreased by lorazepam and chlorpromazine in a dose-dependent manner, with corresponding changes seen in VARS [19].
• Effect of the UGT2B15 genotype on the pharmacokinetics, pharmacodynamics, and drug interactions of intravenous lorazepam in healthy volunteers [20].

Anatomical context of Ativan

• RESULTS: Lorazepam significantly attenuated the BOLD-fMRI signal in a dose-dependent manner in bilateral amygdala and insula but not in the medial prefrontal cortex [12].
• Lorazepam did not affect the BOLD-fMRI signal in the primary visual cortex [12].
• The thalamus as the generator and modulator of EEG alpha rhythm: a combined PET/EEG study with lorazepam challenge in humans [21].
• The distributed MRI-constrained MEG source estimates demonstrated decreased alpha (10 Hz) activity in and around the parieto-occipital sulcus and in the calcarine sulcus of the occipital lobe, following from increased GABA(A)-inhibition by lorazepam [22].
• Whereas the normal and alcoholic subjects showed similar responses to lorazepam in occipital and cerebellar metabolism, the alcoholic subjects showed significantly less of a response than the comparison subjects in the thalamus, basal ganglia, and orbitofrontal cortex [23].

Associations of Ativan with other chemical compounds

• The odds ratio was 1.9 (95 percent confidence interval, 0.8 to 4.4) in the lorazepam group as compared with the diazepam group and 2.3 (95 percent confidence interval, 1.0 to 5.9) in the diazepam group as compared with the placebo group [1].
• We studied the effects of a high-affinity gamma-aminobutyric acid (GABA)-benzodiazepine-receptor agonist (lorazepam) and an antagonist (flumazenil) in humans, using H2(15)O positron-emission tomography [24].
• BACKGROUND: Purpose of this study was to investigate the functional relationship between electroencephalographic (EEG) alpha power and cerebral glucose metabolism before and after pharmacological alpha suppression by lorazepam [21].
• CONCLUSIONS: Results of this work suggest that longterm use of haloperidol, thioridazine, and lorazepam in nursing homes to manage agitation should be closely monitored for their efficacy [25].
• Effect of oral contraceptives on triazolam, temazepam, alprazolam, and lorazepam kinetics [26].
• Paradoxically, patients pretreated with lorazepam even needed more propofol in the early phase of sedation (275+/-39 vs 159+/-37 microg/kg in minutes 5-10, P<.05) and the total amount of ketamine administered was higher in this group as well (15.8+/-1.4 vs 11.3+/-1.2 microg/kg/min, P<.05) [27].

Gene context of Ativan

• Decreased GABAA receptor subunit mRNA concentrations following chronic lorazepam administration [28].
• In cerebral cortex, concentrations of mRNA for the alpha 1 and gamma 2 subunits were unchanged from vehicle or control after 1-10 days of lorazepam [28].
• Administration of 250 micrograms/kg or 500 micrograms/kg lorazepam significantly delayed the onset of secondary potentiation (frequency potentiation) of the population spikes recorded in subfields CA1 and CA3 of the dorsal hippocampus [29].
• 3. Pretreatment of the animals with both Lorazepam and Clonazepam abolished the decrease induced by footshock in MAO A activity in brain [30].
• Five Minute Speech Sample Expressed Emotion (FMSS-EE) was examined in families of youth with depressive disorders, nondepressed youth with attention deficit/hyperactivity disorder (ADHD), and community controls screened for the absence of depression and ADHD [31].

Analytical, diagnostic and therapeutic context of Ativan

• In a randomized, double-blind study, we compared lorazepam with placebo for the prevention of recurrent seizures related to alcohol [32].
• Intravenous lorazepam to prevent nausea and vomiting associated with cancer chemotherapy [33].
• OBJECTIVE: To determine whether lorazepam dose-dependently attenuates blood oxygenation level-dependent functional magnetic resonance imaging (BOLD fMRI) activation in the amygdala and associated limbic structures during an emotion face assessment task [12].
• Ten healthy young subjects were scanned on four occasions, 2 weeks apart; they were administered i.v. saline during two placebo-scanning sessions and then alternately administered i.v. lorazepam (1 mg) or scopolamine (0.4 mg) in a double-blind, randomized, cross-over design [34].
• Lorazepam, a dichloro-3-hydroxy-1,4-benzodiazepine, has been shown to be a potent anticonvulsant in animal models of epilsepsy and has minimal depressant effects on respiration and circulation in humans [35].

References