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Biomedical subjects

B Shapira

Publications and source records attributed to B Shapira.

At least 37 records · Page 2Linked to original sources
PubMed1995

Onset and time course of antidepressant action: psychopharmacological implications of a controlled trial of electroconvulsive therapy.

Onset and time course of antidepressant effect were examined in 47 patients with major depressive disorder who had been randomly assigned to twice weekly bilateral, brief pulse electroconvulsive therapy plus one simulated treatment per week (ECTx2) or to a three times weekly schedule of administration (ECTx3). Rapid improvement was observed in the ECTx3 group in whom the number of real ECTs to 30% reduction on the Hamilton Depression Scale (HAM-D) was 3.2 +/- 1.90, administered over 7.3 +/- 4.43 days and to 60% reduction, 5.9 +/- 3.09 real ECTs over 13.7 +/- 7.21 days. Among the responders in both groups combined, 24.3 +/- 29.58% of the overall improvement in HAM-D was contributed by the first real ECT, 60.9 +/- 28.13% by the first four real ECTs and 91.6 +/- 25.82% by the first eight. Although 85.3% of the responders had reached 60% HAM-D improvement after eight ECTs, a clinically significant minority (14.7%) responded later in the course (ECT 9-12). However, response was predictable on the basis of symptomatic improvement (30% on the HAM-D) by the sixth real ECT. Thirty-three out of 34 responders would have been correctly identified by this criterion and only 2 out of 13 non-responders mis-identified (P < 0.000001). Once achieved, the antidepressant effect was stable, without continuation pharmacotherapy, until 1 week after the last treatment and on lithium carbonate (Li) or Li plus clomipramine for a further 3 weeks. These findings confirm the clinical impression that ECT is a rapidly effective treatment for major depression with a shorter latency than generally reported for antidepressant drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Antidepressant and cognitive effects of twice- versus three-times-weekly ECT.

OBJECTIVE: The purpose of this study was to determine which of the two commonly used schedules of ECT administration, twice or three times weekly, is clinically optimal in terms of antidepressant efficacy and cognitive effects. METHOD: In this double-blind study, 52 consenting, medication-free patients with major depressive disorder, endogenous subtype (Research Diagnostic Criteria), were randomly assigned to bilateral, brief-pulse, constant-current ECT administered over 4 weeks at a rate of three times weekly or twice weekly with the addition of one simulated ECT (anesthesia and muscle relaxant only) per week. Outcome measures were the Hamilton Depression Rating Scale, Acute Cognitive Effects Battery, and Chronic Cognitive Effects Battery. RESULTS: Hamilton depression scale scores were significantly improved by both schedules, with no difference in outcome either 1 week or 1 month after the end of the ECT series. However, the rate of response to ECT three times a week was significantly faster and was related to the rate of real ECT administration. Cognitive effects were more prominent with ECT three times a week. CONCLUSIONS: ECT twice a week is an effective schedule for clinical practice and is potentially advantageous in view of a therapeutic outcome identical to that of ECT three times a week and less severe cognitive effects. ECT three times a week may be specifically indicated when early onset of clinical effect is of primary importance.

Adult↗
PubMed1995

A prospective study of lithium continuation therapy in depressed patients who have responded to electroconvulsive therapy.

Twenty-eight of 34 patients with major depression who completed a course of electroconvulsive therapy (ECT) and were classified as responders were administered lithium carbonate (Li) continuation therapy in the context of an open, prospective study. Twenty-four patients were followed for 6 months or until relapse; four patients dropped out of follow-up while still in remission. The probability of completing 6 months without relapse (by survival analysis, including the patients who dropped out as censored observations) was 65%. The eight patients who relapsed into depression all did so within 13 weeks. They were characterized by a shorter duration of their index depressive episode, a greater likelihood of having suffered an additional depressive episode in the preceding 12 months, and failure of an adequate trial of antidepressant medication before the ECT course. Novel pharmacological strategies may be needed in the post-ECT continuation therapy of patients who have a prior history of relapse and are demonstrably resistant to antidepressant medication.

Combined Modality Therapy↗
PubMed1995

Effects of electroconvulsive therapy on plasma GABA.

There are no published data on the effects of seizures on indices of gamma-aminobutyric acid (GABA) function in human subjects. In study 1, the effects of electroconvulsive therapy (ECT) on free plasma GABA were studied in 39 inpatients with major depressive disorder. Acutely after ECT, free plasma GABA was significantly reduced for up to 1 h after seizure termination, and this finding replicated strongly in a subgroup of six patients who received a second course of ECT. In a second study at a different site that compared sham ECT and real ECT in seven patients, some doubt was raised about the replicability of the acute effect of ECT on GABA levels. Nonetheless, the strength of the findings in the larger study 1 sample suggests that, unlike virtually all other biochemical indices, free plasma GABA may be reduced acutely after ECT. This acute decrease could reflect decreased levels of GABA in brain extracellular space or decreased brain turnover. In study 1, compared with ECT nonresponders, ECT responders had higher GABA levels at both baseline and after a course of ECT. Because plasma GABA levels are known to be low in a subset of patients with major depression, the higher GABA levels observed in clinical responders before and after the ECT course indirectly suggest that patients least abnormal in GABA levels may show superior clinical response. This also suggests that low plasma GABA is not a state marker for depression.

Adult↗
PubMed1993

Prolactin response to fenfluramine and placebo challenge following maintenance pharmacotherapy withdrawal in remitted depressed patients.

Plasma prolactin (PRL) response to fenfluramine (FF) (60 mg orally) and placebo challenge was examined in eight remitted depressed patients who were withdrawn for 14 days from maintenance pharmacotherapy with clomipramine (CMI) plus lithium carbonate (Li) (n = 6) or Li alone (n = 2), 6 months after recovering from their major depressive episode. The patients had undergone identical FF challenge tests while drug free prior to commencing treatment with electroconvulsive therapy (ECT) (n = 4) or CMI supplemented with Li (n = 4) and after completing the above treatments. PRL response to FF in the remitted, drug-free state was significantly enhanced compared to the response prior to treatment (while depressed and drug-free) and not significantly different from the response following treatment with ECT (n = 4) or CMI plus Li (n = 4) 6 months before. Other work of a similar nature supports the view that enhanced serotonergically mediated hormone release in drug-withdrawn, remitted depressives, represents a long-standing change in central serotonergic responsiveness and not a continued effect of antidepressant treatment or a manifestation of medication withdrawal.

Clomipramine↗
PubMed1993

5-HT-1A receptor-mediated effects of antidepressants.

1. Antidepressant (AD) drugs in general induce subsensitivity of behavioural functions associated with activation of 5-HT-1a receptors in animals. 2. Electrophysiological studies in animals in general indicate increased serotonergic transmission after AD administration, mediated partly by increased functioning of post-synaptic 5-HT-1a receptors in the hippocampus. 3. Binding studies have in general shown no change in 5-HT-1a receptor number either pre-or post-synaptically, while results of second messenger studies (inhibition of adenylate cyclase) indicate subsensitivity after AD administration. 4. Human studies also indicate subsensitivity of 5-HT-1a receptors after ADs.

Animals↗
PubMed1992

Effect of clomipramine and lithium on fenfluramine-induced hormone release in major depression.

Prolactin (PRL) and cortisol responses to oral administration of d-1 fenfluramine hydrochloride (60 mg) and placebo were examined in patients with endogenous major depressive disorder on three separate occasions: prior to treatment with clomipramine (CMI), after 4 weeks of CMI administration (175-250) mg/day), and 3 weeks after addition of lithium (Li) carbonate (serum level 0.5-0.9 mmol) to the treatment regimen. CMI significantly increased baseline PRL levels which were further elevated following Li supplementation. PRL response to fenfluramine (minus elevated baseline PRL levels) but not to placebo, was significantly increased by CMI administration, reflected over the 6-hr time course examined and in peak minus baseline values. Following addition of Li, the degree of enhancement was diminished although the peak minus baseline value remained significant relative to the pretreatment response. Cortisol levels were not increased by fenfluramine and were not altered by CMI or CMI + Li administration. The effect of CMI extends previous observations regarding the action of antidepressant treatment on serotenergically mediated hormone release. Methodological considerations relevant to the effect of CMI + Li are discussed.

Adult↗
PubMed1992

Effect of fenfluramine on mood: a double-blind placebo-controlled trial.

Depressed patients (n = 10), schizophrenics (n = 6), and normal control subjects was (n = 9) were administered fenfluramine hydrochloride (FF) (60 mg/os) or placebo in the context of a randomized, double-blind crossover trial. No effect of FF on mood or activation was detected over a 6-hr period. A previous report claiming acute antidepressant effects of FF in depressed subjects was not confirmed.

Adult↗
PubMed1992

Platelet adenylate cyclase activity in depression and after clomipramine and lithium treatment: relation to serotonergic function.

Adenylate cyclase activity was measured in platelet membranes from 10 healthy controls, 12 depressed patients, and the same patients after treatment with clomipramine (CMI) followed by lithium carbonate (Li) supplementation, in an attempt to determine whether any evidence for an effect on the serotonergic system could be obtained in peripheral cells. There were no differences in basal, NaF-, PGE1-, or forskolin-stimulated activity either between the control subjects and depressed patients or between activities in the patients measured before treatment, after CMI, and after CMI+Li. The degree of inhibition of forskolin-stimulated adenylate cyclase by 5-HT, an effect putatively mediated by a 5-HT1A-like receptor, was not different in the depressed patients compared to controls or affected by CMI treatment, but was significantly reduced after Li supplementation.

Adenylyl Cyclases↗
PubMed1992

Hormone responses to fenfluramine and placebo challenge in endogenous depression.

Plasma prolactin and cortisol levels after oral administration of d-l fenfluramine hydrochloride (60 mg) and placebo were examined in 24 endogenously depressed patients and 21 age- and sex-matched normal control subjects in a randomized, double-blind study. Prolactin levels were significantly increased by fenfluramine in both groups, but the response was significantly blunted in the depressed patients compared with the controls. This effect was partially dependent upon elevated baseline cortisol levels in the depressed group and was also influenced by a history of weight loss. Plasma cortisol levels were not increased by fenfluramine in either group. These findings confirm previous reports and suggest that patients with endogenous major depression are characterized by central serotonergic hyporesponsivity. The need to account for baseline effects on hormonal responses to putative serotonergic agents is supported by the findings; however, these effects appear to be less striking when endogenicity is a prominent clinical feature of the depressive syndrome. The apparently complex influence of weight loss on prolactin response to serotonergic challenge remains to be clarified as well as the role played by the bioavailability of the challenge drug and its metabolite.

Adult↗
PubMed1992

Enhanced serotonergic responsivity following electroconvulsive therapy in patients with major depression.

Prolactin release in response to fenfluramine hydrochloride (60 mg orally) and placebo was evaluated in 18 medication-free patients with RDC major depressive disorder, endogenous subtype, before and after a series of bilateral treatments with ECT. Before ECT, fenfluramine induced a twofold increase in plasma prolactin levels. This response was significantly enhanced after the ECT series, while baseline prolactin levels and response to the placebo challenge were not altered. There was no significant difference in plasma fenfluramine and norfenfluramine levels during the pre- and post-ECT challenges. These findings suggest that ECT enhances central serotonergic responsivity and extend to depressed patients pre-clinical observations regarding the effect of electroconvulsive shock on serotonergic function.

Depressive Disorder↗
PubMed1992

Regulation of 5-hydroxytryptamine1A receptor function in rat hippocampus by short- and long-term administration of 5-hydroxytryptamine1A agonist and antidepressants.

Single s.c. injections of the 5-hydroxytryptamine (5-HT)1A receptor agonists buspirone at 4 mg/kg, 8-hydroxy-2-(di-n-propylamino)tetralin at 1 or 4 mg/kg or ipsapirone at 10 mg/kg did not affect 5-HT inhibition of forskolin-stimulated adenylate cyclase activity in rat hippocampal membranes. However, a single injection of buspirone at 8 mg/kg, and daily injections of each of the agonists for 8 days, resulted in a reduction in the degree of enzyme inhibition by 5-HT. Chronic administration of the antidepressants fluoxetine, zimelidine and maprotiline by i.p. injections at 15 mg/kg for 3 weeks also resulted in a decreased degree of enzyme inhibition. Chronic iprindole at the same dose had no effect. It is concluded that the antidepressant-like properties of 5-HT1A receptor agonists may be mediated partly by a postsynaptic action at the level of serotonergic second messenger transduction in the hippocampus.

Adenylyl Cyclases↗
PubMed1991

Effects of lithium and desimipramine on second messenger responses in rat hippocampus: relation to G protein effects.

The effects of chronic administration of lithium, short-term administration of lithium, chronic administration of DMI and a combination of short-term administration of lithium and chronic administration of DMI on second messenger responses were studied in the hippocampus of the rat. Lithium reduced the ability of carbachol to inhibit forskolin-stimulated activity of adenylate cyclase in hippocampal membranes but had no effect on carbachol-stimulated formation of inositol phosphate in hippocampal slices. Lithium, however, reduced the degree of stimulation of formation of inositol phosphate, induced by noradrenaline. Desimipramine alone did not affect carbachol- or noradrenaline-mediated reactions and a combination of short-term administration of lithium and chronic administration of DMI did not potentiate the action of lithium on adenylate cyclase. Both lithium and DMI abolished the inhibition by 5-HT of carbachol-stimulated formation of inositol phosphate a 5-HT1A receptor-mediated response. It is concluded that the chronic effects of administration of lithium may be related to actions at the G protein level and that different modes of coupling of receptors to G proteins may be responsible for the variety of effects observed.

Adenylyl Cyclases↗
PubMed1991

Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions.

Twenty-seven medication-free, depressed patients (Research Diagnostic Criteria, endogenous subtype) were administered a comprehensive battery testing memory and other cognitive functions before and after a series of bilateral, brief-pulse electroconvulsive therapy (ECT) administered according to a dosage-titration procedure (8.9 +/- 1.981 treatments). A subset of patients (N = 14) were reexamined at 1 month and 6 months after the conclusion of the treatment. Anterograde (verbal and visuospatial tasks), as well as retrograde (famous and personal events), memory function was significantly impaired at the end of the ECT series. By 1 month follow-up, performance had improved to pre-ECT (depression) levels on both anterograde and retrograde tasks and exceeded these by 6 months. The memory deficits induced by ECT were not a consequence of generalized cognitive impairment. Furthermore, depression and ECT were shown to independently affect memory, and recovery from depression was not a consequence of the amnestic action of the treatment. The results generally confirm previous reports regarding the nature of ECT-induced memory impairment, in a different language and culture. They suggest that long-term effects of the treatment on memory are even less prominent than previously observed.

Adult↗
PubMed1991

Optimal use of electroconvulsive therapy: choosing a treatment schedule.

Choice of treatment schedule is an important component of the ongoing efforts to optimize electroconvulsive therapy (ECT) administration and thereby maximize therapeutic benefit while reducing cognitive adverse effects. Frequency of ECT administration (that is, the spacing between treatments) and the total number of treatments in a series are the two factors that define the ECT schedule. Available evidence supports the view that a schedule of twice weekly ECT with a total of six to eight treatments is an effective therapeutic regiment that potentially reduces cognitive morbidity associated with more frequent administration and a larger number of treatments. More frequent administration, however, may accelerate antidepressant response and may be indicated in cases in which rapidity of therapeutic effect is a significant clinical consideration. This consideration may be at the cost of greater cognitive impairment, which could be reduced by limiting the number of treatments administered. Aside from their clinical relevance, these issues have important implications for understanding the mechanisms of action of ECT.

Depressive Disorder↗