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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent reports of reduced seizure duration with ECT under propofol anaesthesia have led to concerns that propofol may diminish the efficacy of this treatment. To investigate the effect of propofol on the response to ECT, we reviewed records of 66 patients with primary depression treated with ECT, 37 of whom had been assessed prospectively with pre- and post-ECT Hamilton and Zung depression severity ratings. Despite demonstrating that the individual seizure duration was significantly reduced with propofol compared to thiopentone we found no evidence of reduced ECT efficacy with propofol. Courses under propofol anaesthesia were on an average two treatments longer than with thiopentone. Although this difference was not statistically significant this may have been due to a type II error. These results suggest that it is premature to abandon the use of this new anaesthetic agent in ECT without controlled prospective outcome studies.
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PMID:Propofol as an anaesthetic agent for ECT: effect on outcome and length of course. 187 62

In a random-assignment, double-blind, controlled comparison in 38 melancholic men, overall antidepressant potency of high-dose electroconvulsive therapy (378-mC charge) given with right unilateral electrode placement was not significantly different from that with bilateral placement, although there was a trend for faster improvement with bilateral ECT. The suprathreshold character of the stimulus, about 2.5 times the expected seizure threshold, may have contributed to the high efficacy of brief-pulse right unilateral electroconvulsive therapy found in this study.
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PMID:Antidepressant effects of high-dose right unilateral electroconvulsive therapy. 188 58

In a randomized, double-blind, placebo-controlled pilot study of 40 depressed inpatients, the authors compared two techniques for maintaining seizure duration during pulse unilateral ECT: pretreatment with intravenous caffeine versus electrical stimulus intensity dosing. Both techniques effectively maintained seizure duration, but with caffeine this was accomplished without any increase in mean stimulus intensity over the course of ECT. There were no differences between the two techniques in therapeutic outcome or cognitive side effects from ECT, and caffeine pretreatment was well tolerated. The authors discuss the clinical and research implications of these findings with respect to strategies for maintaining seizure duration during ECT.
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PMID:Caffeine augmentation of ECT. 153

This report describes the investigation of a spontaneous grand mal seizure in a 55-year old woman, being treated with drugs and ECT for depression. The spontaneous seizure was due to hyponatremia caused by self-induced water intoxication, although psychotrophic medication may have contributed by lowering the seizure threshold. The diagnosis of hyponatremia is discussed.
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PMID:Hyponatremic seizure following ECT. 250 79

Status epilepticus is a rare complication of ECT. We describe a patient who suffered a prolonged seizure which required termination with intravenous diazepam. The status epilepticus was not accompanied by motor movements, and the diagnosis was made only because of simultaneous EEG monitoring. The incidence of status epilepticus after ECT may be underestimated.
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PMID:Status epilepticus after electroconvulsive therapy. 260 16

Primary care physicians have a vital role to play in identifying depression in their elderly patients. Diagnosis may be difficult, because symptoms are atypical and frequently include psychomotor agitation, somatic symptoms, and complaints of memory loss. Patients with medical illnesses, such as cancer, postmyocardial infarction, stroke, Parkinson's disease, and early Alzheimer's disease are particularly vulnerable to depression. Drugs that may cause depressive symptoms are digitalis at toxic levels, beta-blockers, centrally acting antihypertensives, immunosuppressants, and nonsteroidal anti-inflammatory agents. Cyclic antidepressants are the drugs of first choice. Selection depends on the patient's physical health and current medications and the side effect profile of the drug. Side effects are more pronounced in old age because of drug accumulation owing to slowed clearance. Troublesome side effects are anticholinergic effects, orthostatic hypotension, sedation, cardiotoxicity, and weight gain. The most useful antidepressants for geriatric patients are the secondary amines, desipramine and nortriptyline. The second-generation drug trazodone has the advantage of causing the least anticholinergic effects, but it is very sedating. Before treatment, the patient should have an electrocardiogram, liver function tests, tonometry, sitting and standing blood pressures, evaluation of urinary symptoms for outflow obstruction, review of current medications, and estimation of suicide risk. Cyclic antidepressants are contraindicated during recovery from myocardial infarction, in heart disease when there is severe impairment of myocardial performance, in seizure disorders, and in the presence of glaucoma or a large prostate. Drug interactions that may cause trouble can occur with epinephrine, MAO inhibitors, thyroid hormone, cimetidine, and centrally acting antihypertensives. Dosage should start low, increasing usually by 25 mg every 4 to 5 days until a therapeutic level is reached. Failure of a noradrenergic antidepressant after 4 to 5 weeks can be followed by a trial of a serotonergic drug. Drug serum level monitoring is useful for imipramine, desipramine, and nortriptyline. Monoamine oxidase inhibitors are effective in many elderly patients who are resistant to TCAs. Sympathomimetic drugs must be avoided with MAOIs. Elderly patients are at high risk of toxicity and drug interactions with lithium. Electroconvulsive therapy is useful for patients who do not respond to drug treatment, but medical complications, particularly cardiovascular, often occur in patients 75 or older. Many patients relapse after ECT. Psychotherapy together with pharmacotherapy may be the optimal treatment for elderly depressives. Older patients are more likely to become chronically depressed than younger patients. The risk of suicide in depressed elderly males is high, particularly in those with psychosocial problems, and depression rises with age.
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PMID:Management of depression in the elderly. 266 41

Electroconvulsive therapy can produce severe disturbances in the cardiovascular system, most commonly a transient period of hypertension. This study was designed to determine whether propofol, in comparison with methohexital, would attenuate this hypertensive response. Fifteen patients were studied during courses of six ECT administrations, each patient receiving propofol or methohexital on different occasions. Arterial pressure, heart rate, and cardiac rhythm were recorded. The induction doses were 1.08 +/- 0.03 mg.kg-1 of methohexital, and 1.60 +/- 0.04 mg.kg-1 of propofol. Systolic pressure, diastolic pressure, and heart rate were consistently lower following propofol than methohexital (P less than 0.005). The mean maximum increase over baseline systolic pressure was 2.1 +/- 2.9 mmHg with propofol, and 26.7 +/- 4.5 mmHg with methohexital (P less than 0.001). Cardiac rhythm abnormalities were infrequent, and their incidence did not differ significantly between the two induction agents (P greater than 0.3). The duration of seizures, as measured clinically, was reduced with propofol (17.9 +/- 2.5 s) in comparison with methohexital (30.9 +/- 2.8 s) (P less than 0.001). Recovery times were similar for the two agents. Since the role of seizure duration in the therapeutic efficacy of ECT remains controversial, propofol may be a useful induction agent for this procedure.
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PMID:Comparison of methohexital and propofol for electroconvulsive therapy: effects on hemodynamic responses and seizure duration. 278 92

The EEG has been a widely-used screening procedure before ECT. Previous studies have correlated seizures and post-ECT slowing with ECT efficacy. We investigated the utility of pre-ECT EEG in predicting therapeutic response and post-ECT confusion. EEGs were normal in 54 of 100 patients undergoing first courses of ECT for refractory depression. Patterns within the normal range, were present in 26/100 while 2/100 had paroxysmal discharges without clinical evidence of epilepsy. Focal and generalized EEG slowing were each present in 9/100 records. Full recovery occurred after ECT in 66.6 per cent of those with normal pre-ECT records, 61.5 per cent with borderline EEGs, 55.5 per cent of patients with diffuse EEG slowing, and 22.2 of cases with focal slow waves. Of those with EEG slowing 22.2 percent had little or no response to ECT as compared to 19.2 per cent with EEGs within normal limits and 9.3 per cent with normal EEGs. Four of 6 patients with prolonged confusion had normal EEGs, while 1 each had focal and generalized slowing. EEG slowing was related to incomplete ECT response, but not to therapeutic failure or post-ECT confusion. The limited predictive power of pre-ECT EEG may reflect the prevalence of normal or nonspecifically abnormal EEGs in psychiatric patients and the general efficacy of ECT. Other neurophysiologic methods may yield more definitive information about the mechanism and use of ECT.
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PMID:Predictive value of electroencephalography for electroconvulsive therapy. 292 28

Platelet alpha 2-and lymphocyte beta 2-adrenoceptor densities, plasma noradrenaline and serum cortisol were measured before, during and one week after a course of EEG-monitored electroconvulsive therapy, in nine depressed patients. A 50% fall in Hamilton Depression Rating scores occurred after a fairly consistent total seizure time, regardless of the amount of ECT given. Platelet alpha 2-adrenoceptor densities showed a statistically significant fall after three ECTs, but were unchanged after the full course of ECT and were independent of clinical change. Lymphocyte beta 2-adrenoceptor densities were unaltered. Plasma noradrenaline concentrations were initially high, and fell with ECT in a manner paralleling clinical recovery. Plasma noradrenaline may be a more useful index of central changes during antidepressant treatment than peripheral blood cell receptor densities.
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PMID:Adrenergic receptors in depression. Effects of electroconvulsive therapy. 299 28

The generation of the spike-wave activity of Phase III of ECT seizures is attributed to the recurrence of synchronized, prolonged periods of intense inhibitory current flow (hyperpolarization), and associated rebound spike bursts, produced by the inhibitory circuit relationships and intrinsic electrophysiological properties of thalamic neurons. An anatomical and neurophysiological model of the development of generalized, synchronous 3-Hz spike-wave seizure activity is proposed which outlines the origin, maintenance, slowing, and termination of this fundamental seizure rhythm. Phase III inhibitory current flow (delta energy) and/or spike bursts may bring about therapeutic benefit by initiating a chain of agonist-independent and agonist-dependent events which results in long-term augmentation of serotonergic and noradrenergic neurotransmission and diminution of cholinergic neurotransmission in the forebrain. A specific anatomical and functional model of the mechanism of action of ECT is proposed, in which: (1) adrenergic and cholinergic pathways in the forebrain are assumed to be massively stimulated during ECT seizures, whereas serotonergic pathways are assumed to be inhibited during these seizures; (2) the beneficial effects of ECT are considered to be more dependent upon ECT-induced changes in 5-HT neurotransmission than upon alteration of noradrenergic function; (3) these beneficial effects involve up-regulation of 5-HT2 and down-regulation of M1- and M2-muscarinic receptor densities by both agonist-independent and agonist-dependent mechanisms, coupled with functional augmentation of noradrenergic neurotransmission; and (4) these effects may be brought about by Phase III inhibitory current flow- and/or spike burst-induced alteration of the function of second-messenger generator systems.
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PMID:The electroencephalographic pattern during electroconvulsive therapy: V. Observations on the origins of phase III delta energy and the mechanism of action of ECT. 306 Feb 88


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