Sir: Mirtazapine is classed as a noradrenergic and specific serotonergic antidepressant (NaSSA). It acts by blocking α 2 receptors on noradrenergic neurons and enhancing norepinephrine release. 1 Increased levels of norepinephrine act on α 1adrenoceptors on serotonergic cell bodies, increasing serotonergic firing. 1 Nightmares occur only in rapid eye movement (REM) sleep. Most antidepressants suppress REM sleep; hence, nightmares are not a commonly reported side effect of therapy with antidepressants. We report the first ever case, to our knowledge, of a patient who developed severe nightmares on initiation of therapy with mirtazapine, which necessitated stopping the drug.Case report. Mr. A, a 52-year-old white man, presented in 2006 with depressive symptoms including low mood, poor sleep and appetite, loss of weight, hopelessness, and fatigue. Because of his symptom profile, he was started on mirtazapine, 15 mg at night. One day later, he reported vivid nightmares of being murdered and his body being cut up. These nightmares woke him from sleep and left him feeling very scared and upset. He recalled that he had been treated with mirtazapine 2 years ago and it had to be discontinued because of similar distressing nightmares. After 4 days of therapy and experiencing nightmares every night, he requested that the medication be stopped.
The actions of sodium 4-hydroxybutyrate, y-aminobutyric acid and meprobamate have been studied in unanaesthetized animals, in local anaesthetic tests, on isolated organ preparations, on convulsions induced by picrotoxin and strychnine, and on monosynaptic (patellar) and polysynaptic (plantar) reflexes of the spinal cord. Sodium 4-hydroxybutyrate induced a sleep-like state with three unusual features: the righting reflex was remarkably persistent, respiration was good throughout and recovery was abrupt. y-Aminobutyric acid was inactive and meprobamate caused flaccid paralysis with loss of the righting reflex. None of the agents affected the responses of the rat diaphragm either to direct stimulation of the muscle or to indirect stimulation through the phrenic nerve. Only meprobamate reduced the responses of the guinea-pig isolated ileum preparation, showed local anaesthetic action and had an anticonvulsant action. All three compounds were capable, after intravenous or topical application, of blocking plantar reflexes in doses which did not affect the patellar reflex. The spinal animal responded in the same way, to the same dose of sodium 4-hydroxybutyrate, as the decerebrate preparation. Topical application to the motor cortex had no effect on spinal reflexes. We conclude that sodium 4-hydroxybutyrate acts preferentially on the internuncial neurones in the spinal cord but differs from meprobamate in its other actions. The similarity between the actions of sodium 4-hydroxybutyrate and of y-aminobutyric acid provides further evidence in support of the hypothesis that sodium 4-hydroxybutyrate is involved in the y-aminobutyric acid metabolic pathways.
Animals given substances with thyroid activity show a reduced resistance to anoxia (Duran, 1920), and Smith, Emmens, and Parkes (1947) have used this effect in a method of thyroid assay based on the survival times of mice in closed jars. We have used it for comparing the activities of thyroxine and some of its derivatives. We find it relatively simple to carry out; the results it gave have been confirmed in clinical trials, both with sodium thyroxine and with the N-formyl derivative (Hart and Maclagan, 1950).We were particularly interested in two questions: has solubility an important effect on the activity of thyroxine and has thyroxine enhanced activity in the dried glandular extract ? For this purpose a number of preparations of synthetic thyroxine and its derivatives were prepared (Clayton and Hems, 1949) and examined for thyroid activity. This paper records the results obtained biologically. PROCEDURE Throughout the whole of the experiment the mice were kept in a thermostatically controlled incubator room at a temperature of 25.50 ± 1°. For each experiment use was made of male fawn mice of the GFF strain, weighing between 18 and 24 grammes, distributed into groups of twenty animals to give uniform body weight representation. Usually six groups, at ascending dose levels, were employed, three for the standard and three for the test preparations; a further twenty mice were kept as controls.The doses were administered on three alternate days, every animal in a group receiving the same dose irrespective of body weight and the volume of the solution injected being the same for all groups. All compounds for assay were either suspended in 0.9 per cent sodium chloride solution or dissolved in 0.01 M-sodium carbonate solution containing 0.9 per cent sodium chloride.On the second day after the final injection the groups of ten mice were sealed in glass jars and the time of sealing was recorded. We used 32-oz. wide neck, screwcapped clear bottles, with soft paraffin smeared on the neck to ensure a complete seal. The volumes of the jars ranged from 980 to 1,020 ml., and they were randomly distributed. The time of survival was recorded for each individual mouse, the endpoint being the last visible respiration, which is almost invariably preceded by marked terminal convulsions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.