Effects of propofol on electroconvulsive therapy seizure duration (original) (raw)
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Psychiatric Syndromes Related to Antiepileptic Drugs
Epilepsia, 1999
All antiepileptic drugs may provoke positive or negative psychiatric reactions in individual patients. These psychotropic effects are not simply idiosyncratic but depend on the drug's anticonvulsive strength and the person's genetic and biographic psychiatric predisposition. Mechanisms related to psychiatric adverse events are polytherapy and folate deficiency, forced normalization, drug toxicity, and withdrawal. Our knowledge on dose independent, idiosyncratic psychotropic side effects is still limited. With respect to the older antiepileptic drugs there are almost no systematic data, and knowledge is largely empirical and based on anecdotal reports. With respect to the new generation of anticonvulsants there are data on psychiatric side effects from drug trials. However, these data are not always entirely transparent to the interested epi-leptologist. Moreover, drug trials are designed to test anticonvulsive efficacy and psychiatric adverse events are not systematically reported, thus severity psychopathologic nature of behavioral problems remain obscure. Differences in patients included in trials do not allow comparisons of psychiatric risks of specific drugs, particularly since following the vigabatrin experience, patients with a psychiatric history were often excluded from trials. In this chapter, methodological issues related to data on psychiatric adverse events of AED are discussed followed by an overview on the current knowledge on psychiatric side effect profiles of old and new antiepileptic drugs.
Mood effects of antiepileptic drugs
Epilepsy & Behavior, 2004
This article reviews our knowledge about a specific subgroup of chronic CNS-related side effects of antiepileptic drugs (AED) treatment, i.e., the effects of AEDs on mood. In line with a recent hypothesis, using the experience of AED treatment in psychiatry, we examined whether mood effects are related to the known anticonvulsant mechanisms of action of the AEDs. Specifically we examined whether AEDs, acting through potentiation of GABAergic neurotransmitter release, have ''sedating'' effects on mood, whereas AEDs that act through the reduction of excitatory glutamate neurotransmitter release have ''activating'' effects on mood. The results of this review yield evidence that there are relationships between the known anticonvulsant mechanisms of action of the AEDs and mood effects. Mood effects occur especially when the drugs have a sustained effect on neuronal mechanisms, in particular when the inhibitory or excitatory neurotransmitter release is altered. Drugs with ''use-dependent'' impact on sodium or calcium channels probably have a more transient impact and do not lead to interictal stable mood effects. Drugs with multiple mechanisms of action seem to combine a favorable efficacy profile with an increased risk of severe mood problems. The quality of the evidence, however, is not conclusive and there are many paradoxical results. One reason for this lack of ''fit'' may be the use in this review of a simplified classification, based only on the predominant mechanism of action to classify a drug. Only a limited number of AEDs (ethosuximide, tiagabine) are characterized by a single anticonvulsant mechanism of action. Probably more detailed coupling of mechanisms of action (e.g., inspecting the type and route of impact on GABA release) and mood effects may give less confusing results. The use of magnetic resonance imaging techniques such as spectroscopy may provide interesting results.
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2013
Objective: To compare the effects of propofol and etomidate on the stimulus variables and efficacy of electroconvulsive therapy (ECT) in depressed inpatients. Method: This retrospective study included 54 inpatients (aged 18-75 years) who met the DSM-IV criteria for major depression and were treated with bilateral ECT. For the first part of the study, the primary outcome was the mean stimulus charge per ECT session. For the second part, the main outcome measure was the proportion of patients achieving full remission. Results: Propofol-treated patients showed a higher mean stimulus charge (etomidate = 227.58 ± 130.44, propofol = 544.91 ± 237.56, p b 0.001) despite the lack of a significant difference in starting threshold doses. The propofol group had shorter mean electroencephalogram (etomidate = 69.41 ± 22.50, propofol = 42.95 ± 22.26, p b 0.001) seizure duration and motor (etomidate = 46.11 ± 14.38, propofol = 22.89 ± 7.13, p b 0.001) seizure duration and a higher mean number of inadequate seizures (etomidate = 0.12 ± 0.15, propofol = 0.47 ± 0.26, p b 0.001). No significant differences were found between the groups for the effects of the anesthetics on the efficacy of ECT. Limitations: Our study is limited by a retrospective design and the small number of patients treated with propofol restricted the sample size. Conclusions: Anesthesia with propofol has a significant reducing effect on seizure duration during the course of ECT which results in more inadequate seizures, despite the use of a higher mean stimulus charge. Regarding the possible effect of the anesthetics on ECT, randomized clinical trials with sufficient power to detect differences are warranted.
Interactions Between Anticonvulsant and Psychoactive Drugs
Epilepsia, 1999
This review considers the relevance of pharmacokinetic interactions between antiepileptic drugs (AEDs) and psychoactive drugs in the treatment of mood disorders in patients with epilepsy. The determination of plasma levels of some of these drugs (mainly the AEDs) has enabled clinicians to evaluate the kinetic modifications during the course of such combined therapies and to adjusting the dosages in cases of subtherapeutic or toxic levels. In general, phenobarbital, phenytoin, and carbamazepine stimulate the catabolic degradation of tricyclic antidepressants (TCAs), and TCAs have an inhibitory effect on the elimination of AEDs. The newer antidepressants that selectively inhibit the reuptake of serotonin (SSRIs), although in different fashions for the different substances (fluoxetine, fluvoxamine, paroxetine) may cause an increase of plasma AED levels through inhibition of the isoenzyme P450 2D6. Similarly, antipsychotics (APs) are more rapidly metabolized when AEDs are co-administered, whereas AED metabolism is scarcely influenced by AP. Finally, plasma levels of tranquilizers are lowered by AED co-therapy. As the concomitant administration of AED and psychoactive drugs becomes increasingly used for treatment of mood disorders in patients with or without epilepsy, therapeutic drug monitoring may be useful in designing correct and rational therapy.
Seizures with neuroleptics and antidepressants
General Hospital Psychiatry, 1987
Seizures remain among the most serious side effects of psychotropic drugs. The authors review the literature associating neuroleptic and antidepressant medications with seizures, discussing the relative "seizurogenicity" of different medications, risk factors for seizures, and drugs of choice for high-risk patients. Case histories are presented. Available evidence suggests that molindone, fluphenazine, and haloperidol areamong the least seizurogenic neuroleptics and fhat doxepin, monoamine oxidase inhibitors, or electroconvulsive therapy may be safest in treating the depressed patient at risk for seizures.
Ondansetron in the treatment of antidepressant-induced nausea
Journal of the American Psychiatric Nurses Association, 2001
In the next two issues of the journal, Psychobiology Perspectives will feature content in a somewhat different area than previously covered here. We will examine the underlying biology of two sets of problematic side effects from one class of antidepressants, namely those with strong 5-HT2 antagonist properties. Although the mechanism of action of 5-HT2 antagonism has many benefits, it may also yield some untoward effects. Two of these
Epilepsy & Behavior, 2016
For a long time, there has been a misconception that all antidepressant drugs have proconvulsant effects. Yet, antidepressants of the selective serotonin reuptake inhibitor (SSRI) and serotonin-norepinephrine reuptake inhibitor (SNRI) families have been not only shown to be safe when used in patients with epilepsy (PWE) but have been found to display antiepileptic properties in animal models of epilepsy. In humans randomized to SSRIs vs. a placebo for the treatment of primary major depressive episodes, the incidence of epileptic seizures was significantly lower among those treated with the antidepressants. On the other hand, SSRIs and SNRIs can display proconvulsant properties at toxic doses. This article reviews the preclinical and clinical data of antiepileptic and proconvulsant properties of these drugs and addresses special considerations to take when prescribing them for PWE.
Propofol and Methohexital as Anesthetic Agents for Electroconvulsive Therapy
Journal of Ect, 2007
Background: Propofol is often used as an anesthetic agent for electroconvulsive therapy (ECT). Whether the relatively short seizure duration, resulting from the medication, deteriorates the seizure quality and therapeutic outcomes, or whether propofol might be associated with small but significant post-ECT cognitive impairments, is still a subject of controversy. The purpose of our study was to test these hypotheses in comparison with methohexital. Materials and Methods: In a double-blind, controlled study, 50 patients with severe major depression who were to be treated with ECT were randomly assigned to anesthesia with propofol (120.9 T 50.0 mg) or methohexital (83 T 26.3 mg) and were observed for 2 months. The 2 drugs were compared on the basis of electroencephalography-registered seizure duration, mean blood pressure, as well as pulse frequency, seizure efficacy index, and postictal suppression. Systolic and diastolic blood pressure, and seizure duration and quality were recorded consecutively during ECT treatments. Changes in depressive symptoms and cognitive functions were measured at 5 time points, pre-ECT, after the third to fifth ECT, post-ECT treatment, and at a follow-up examination 2 and 8 weeks after the last ECT treatment. Results: Patients on propofol showed a significantly lower increase in blood pressure post-ECT (P G 0.001), their seizure duration was comparable to patients on methohexital (P = 0.072), and seizure quality was significantly superior, as was measured by the Postictal Suppression Index (P = 0.020), and comparable to the methohexital group as measured by the Seizure Efficacy Index (P = 0.160). The improvement of depressive symptoms and the improvement in cognitive functions were similar in both groups (with the exception of the results from 2 cognition tests). Conclusions: Propofol, as compared with methohexital, results in a more moderate increase in blood pressure and shorter seizure duration. The seizure quality did not differ significantly between the 2 groups. We detected a tendency toward improved cognitive performance after anesthesia with propofol as compared with methohexital, but with statistical significance in only 2 cognition trials. Therefore, propofol is a safe and efficacious anesthetic for ECT treatment.