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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The unilateral and bilateral therapy differ in psycho-organic effects but have the same antidepressive efficiency. This is due to the facts that the organic effects are mainly caused by the electrical current whereas the antidepressive effect is dependent on the seizure activity. Compared to the bilateral treatment, unilateral gives reduced confusion, anterograde and retrograde amnesia as well as reduced experience of memory impairment. The difference is explained by a lower density of current in the brain. The unilateral treatment should be the treatment to be chosen. The antidepressive action of ECT fits the amine hypothesis, ECT causes a sustained increase of the synthesis of norepinephrine and of the sensitivity of amine receptors and creates conditions for alleviating both "low-output" and "low-sensitivity" depression. The antidepressive action is probably mediated by release of hypothalamic neurohormones.
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PMID:[Unilateral and bilateral shock therapy: mechanism of action (author's transl)]. 4 67

We have studied the effect of i.v. flumazenil 0.01 mg kg-1 on the amnesia and sedation caused by midazolam 2 mg and 5 mg i.v. in volunteers in order to determine the relationship between the actions of the antagonist on these two effects. Midazolam caused dose-dependent central neural depression as assessed by critical flicker fusion frequency, and dose-dependent amnesia for word cards. In subjects given flumazenil 5 min after administration of midazolam, fusion frequency readings and memory were restored to levels comparable to those before midazolam administration. These two effects of flumazenil were similar in time course and extent, suggesting that they share the same mechanism of action. Flumazenil given alone had no effect on memory. The study has demonstrated anterograde amnesia following benzodiazepine administration and antagonism by flumazenil. There was neither retrograde amnesia nor retrograde antagonism of amnesia.
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PMID:Effect of flumazenil on midazolam-induced amnesia. 222 35

The evidence accumulated so far indicates that seizure activity exerts profound changes on the metabolism of opioid peptides in the hippocampus. Our data consistently show a large transient decrease in dynorphin and a modest decrease in enkephalin in the hippocampus following either a single ECS or KA injection. These initial reductions, which are indicative of increased release, may trigger the biosynthetic process of hippocampal opioids and result in an overproduction of the peptides seen in the rebound phase. However, the amount and timing of the rebound in enkephalin and dynorphin levels in response to repeated ECS, amygdaloid kindling, or KA differ drastically: a rapid and sustained increase in ME-LI follows all three treatments, in contrast to a slow recovery after a large and sustained decrease in DN-LI induced by repeated ECS and amygdaloid kindling. These results, which are unique to the hippocampus, suggest that differential mechanisms are operative in regulating the metabolism of these two opioid peptides in the hippocampus. It is likely that a well-coordinated regulation of hippocampal function can be achieved through the differential release of enkephalin and dynorphin and their subsequent interactions at different subtypes of opioid receptors following seizure activities. From a functional point of view, our data provide a neurochemical correlate of previous reports that brain opioid peptides may mediate ECS-induced behavioral alterations, such as changes in seizure threshold, postictal depression, and retrograde amnesia. The robust changes in the levels of opioid peptides in kindled rats, plus shortening of the kindling process by pretreatment with mu opioid antagonists, strongly suggest the involvement of brain opioid peptides in the development of kindling. Finally, these studies show clear evidence that enkephalin in the hippocampus is important in KA-induced WDS, a component of the opiate withdrawal syndrome in rodents (Isaacson and Lanthorn 1981). Further studies should help distinguish the regulatory mechanisms responsible for changes in opioid peptide metabolism during states of hyperexcitability in the hippocampal formation.
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PMID:Seizure-induced alterations in the metabolism of hippocampal opioid peptides suggest opioid modulation of seizure-related behaviors. 289 42

Antero- and retrograde amnesia are observed as side effects of most types of benzodiazepines. They have rarely been investigated with respect to physical and personality factors, or to prior experiences, present expectations, and emotional states of the subjects, all of which are well known to modify drug response. By reviewing research on benzodiazepine-induced changes of memory in preoperative, anxious, and depressed patients as well as in healthy subjects, it is demonstrated that differences in benzodiazepine-induced amnesic effects may depend on: 1. subject variables like predrug level of anxiety, depressive symptomatology, memory capacity, experiences with benzodiazepine-type drugs, and expectations of treatment outcome, and secondary factors like social environment and treatment setting 2. interactions between these subject variables and type of schedule (times of acquisition, treatment, and testing), type of learning material, and dose of drug. 3. the extent of benzodiazepine-induced changes in anxiety or depression, cortical and emotional arousal (alertness and activity) as well as physiological effects of benzodiazepines Special emphasis should be placed on the investigation of drug-induced changes of covariation between psychological measures which may provide valuable information for differential prediction and on mechanisms of drug action.
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PMID:Individual differences in benzodiazepine-induced changes of memory. 290 10

The influence of synthetic thyrotropin-releasing hormone (TRH) on locomotion, on the effects of analgetics, learning and memory, electrical activity of hypothalamic neurons, blood pressure, and cerebral circulation have been studied. TRH increases the spontaneous motility and potentiates the stimulating effect of amphetamine and apomorphine. It also antagonizes the decrease of motility induced by tetrabenazine in all these tests. TRH exhibits the similarity to antidepressants. TRH antagonizes the effects of morphine and Tyr-D-Ala-Gly-Phe-(NO2)-NH2, especially in respect of respiratory depression experiments made on rats and rabbits. TRH facilitates the learning in active avoidance paradigme, diminishes the degree of retrograde amnesia evoked by maximal electroconvulsive shock. The latter effect suggests that TRH can be considered as a substance having some signs of nootropic activity. TRH seems to interact with central M-cholinergic system. This is evidenced by the ability of atropine to diminish the excitatory effect of TRH applied microiontophoretically to single neurons of the lateral hypothalamus. TRH elevates blood pressure and volume velocity of the cerebral circulation in normotensive animals and recovers the hemodynamics during hemorrhagic hypotension. The spectrum and mechanism of TRH pharmacological activity are discussed. The data suggest that TRH may be of interest for clinical trials.
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PMID:[Pharmacology of thyroliberin]. 641 82

Electroconvulsive shock (ECS) is used in the treatment of depression and causes antero- and retrograde amnesia as a side effect. One of the many neurochemical effects of ECS is depletion of brain beta-endorphin and Met-enkephalin. These two opioid peptides cause antero- and retrograde amnesia also. Naloxone antagonizes the amnestic effect of ECS and of the opioid peptides. Thus, it is possible that the amnestic effect of ECS is mediated by an endogenous release of the peptides. Surgical posterior hypothalamic deafferentation, but not anterior deafferentation or fornix transection, abolishes the amnestic effect of ECS. This suggests that the hyperactivation of endogenous opioid systems by ECS that leads to amnesia is mediated by posterior ascending fibers to the hypothalamus. The relevance of these considerations to the treatment of depression merits investigation.
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PMID:Amnesia as a major side effect of electroconvulsive shock: the possible involvement of hypothalamic opioid systems. 652 15

Experiments on rats and mice were made to study the antianamnestic and antihypoxic effects of some GABA derivatives. Cetyl GABA, sodium and lithium hydroxybutyrates and phenibut were shown to be able to decrease the retrograde amnesia caused by electroshock in passive avoidance performance. As regards the degree of the antianamnestic effect, the above-mentioned non-cyclic derivatives of GABA are not inferior to the standard nootropic drug piracetam, a derivative of cyclic GABA. Antihypoxic activity of sodium hydroxybutyrate, cetyl GABA, phenibut and lioresal studied in experimental hypoxic hypoxia compares very favourably with that of piracetam. The compounds under consideration manifest their protective action against damaging factors in doses which do not provoke muscle relaxation or any types of central depression. According to the data obtained one may conclude that the nootropic effect is exhibited by not only piracetam, a derivative of cyclic GABA, but also by some of its non-cyclic derivatives.
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PMID:[Nootropic properties of gamma-aminobutyric acid derivatives]. 653 1

L-Proline and some of its analogs have been shown to prevent spreading depression (SD) in the chick retina at relatively low concentrations and to impair memory processing without provoking toxic or electrophysiological disturbances. Both effects are hypothesized to be caused by inhibition of the effects of glutamate released into the extracellular space. L-Proline, its D-enantiomer, six proline analogs including two homologs (L-azetidine-2-carboxylic acid and DL-pipecolic acid), and five other compounds were examined for their effects on spreading depression and their amnestic and electrophysiological effects. L-Proline, L-baikiain, DL-3,4-dehydroproline, and L-4-hydroxyproline all reduced the incidence of SD in the chick retina and proved to be amnestic. D-Proline, L-pyroglutamic acid, L-azetidine-2-carboxylic acid, DL-pipecolic acid, L-glutamic acid diethylester, L-isoleucine and L-norleucine neither depressed SD nor caused retrograde amnesia. L-Prolyl-L-proline and L-glutamine did not depress SD at low concentrations but had significant amnestic effects. None of the listed compounds induced EEG disturbances. Implications for memory mechanisms are discussed in the light of these results.
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PMID:Amnestic potency of proline analogs correlates with anti-spreading depression potency. 719 Feb 93

Using the Squire Subjective Memory Questionnaire (SSMQ), depressed patients rated their memory functioning prior to a course of brief pulse, electroconvulsive therapy (ECT) within the 1 week following the course and 2 months later. Normal controls made similar ratings at comparable intervals. Prior to ECT, patients reported poorer memory functioning than controls. There was marked improvements in the patients' self-reports shortly following ECT, and at 2-month follow-up SSMQ scores were generally comparable in patients and controls. At all time points, the severity of depressive symptoms was strongly associated with patients' reports of memory dysfunction. SSMQ subscales ("depression" and "ECT" items) were not differentially sensitive to effects of ECT or depression. Relations between ECT treatment parameters and changes in patients' self-evaluations only emerged after controlling for clinical state change. Shortly following ECT, there were no relations between SSMQ scores and objective measures of cognitive functioning. However, 2 months following ECT, there was a suggestion that greater retrograde amnesia for autobiographical memories was associated with self-rating of greater memory impairment.
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PMID:Subjective memory complaints prior to and following electroconvulsive therapy. 870 66

Twenty patients (mean age 64 years) with a previous episode of transient global amnesia (TGA) were examined to assess the functioning of objective memory (by using the Randt Memory Test), the metamemory capacities (Sehulster Memory Scale), the residual level of retrograde amnesia (Questionnaire of Remote Events), and the level of depression (Geriatric Depression Scale). Patients with residual retrograde amnesia scored significantly lower than non-amnesic ones on indices of both short-term and long-term memory, and for one of three main metamemory components, namely self-rating of memory functioning through comparison with memory functioning of peers (Set3). Age, time interval from TGA attack and TGA duration did not prove to influence memory and metamemory scores. Retrograde amnesia and depression were rather substantially associated (1/5), and this association was found to negatively influence nearly all memory and metamemory scores. Depression level showed a positive correlation with short-term memory functioning in non-amnesics. The different pattern and strength of the relationships between metamemory components and objective memory dimensions observed in amnesics and non-amnesics indicate that metamemory evaluations are more closely related to memory functioning in amnesics than in non-amnesics.
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PMID:Transient global amnesia: memory and metamemory. 883 79


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