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At least 19 recordsLinked to original sources
PubMed1984

Meduna and the origins of convulsive therapy.

Convulsive therapy for dementia praecox was first used by the Hungarian neuropsychiatrist Ladislas Meduna in January 1934. On the 50th anniversary the author discusses the introduction of the treatment, the role of a theory of the biological antagonism between epilepsy and schizophrenia, and the contributions of Meduna, Sakel, Cerletti, and Bini. He also describes the changes in usage and methods and the impact of psychotropic drugs on the practice of convulsive therapy.

Antipsychotic Agents↗
PubMed1985

Electroconvulsive Therapy and Electric Acupuncture Convulsive Therapy in China.

This essay presents briefly the historical development and the present condition of electroconvulsive therapy (ECT) and Electric Acupuncture Convulsive Therapy (EACT) in China. Written on the basis of internal published documents and materials concerning ECT and EACT since 1950 and the clinical experience and experimental research of the authors, it puts forward the authors' views of problems that remain in applying ECT.

Journal Article↗
PubMed1990

Proposals for the mechanism of action of convulsive therapy: a synthesis.

The convulsive therapies have been powerful additions to somatic treatment in psychiatry and have enjoyed widespread application for the benefit of many. A number of theories have been advanced in efforts to account for therapeutic efficacy but none has been comprehensive. These theories can be distinguished by whether they posit a central therapeutic role for stimulation, inhibition, psychological effects, or mixed processes induced by treatment. After critically reviewing extant theories, we propose a model for the effects of the convulsive therapies: Convulsive therapy is essentially nonspecific; "nonphysiological" depolarizations are distinctly important for the restoration of aberrant intravesicular transmitter ratios with resultant therapeusis. We present this model as a working hypothesis that may contribute to the guidance of research in the mechanism of action of convulsive treatment and offer several testable hypotheses in this regard.

Brain↗
PubMed2002

Update on magnetic seizure therapy: a novel form of convulsive therapy.

Magnetic seizure therapy (MST) refers to the use of transcranial magnetic stimulation to induce a seizure for therapeutic purposes. MST is under investigation as a means of improving the safety profile of electroconvulsive therapy (ECT). Although both MST and ECT induce seizures through electrical stimulation of the brain, the electric field induced by MST is more focal and limited than that induced by ECT. Because magnetic fields pass through tissue unimpeded, there is greater control over the site and extent of stimulation with MST than can be achieved with ECT. This enhanced control represents a means of focusing the treatment on target cortical structures thought to be essential to antidepressant response and of reducing spread to medial temporal regions implicated in the cognitive side effects of ECT. MST is currently at an early stage of development. This article reviews the experience with MST in animal models and initial human investigations. Preliminary results have demonstrated the feasibility of performing MST in the clinical setting, and there are suggestions that MST may have advantages over ECT in terms of subjective side effects and some measures of acute cognitive functioning. The antidepressant efficacy of MST is not yet known, but studies designed to address that critical issue are underway. As with all attempts to refine convulsive therapy techniques (such as modifications in stimulation parameter configurations and electrode placement), the ultimate clinical value of MST will need to be established through controlled clinical trials.

Animals↗
PubMed1980

A theory of convulsive therapy in endogenous depression: significance of hypothalamic functions.

The repeated induction of seizures (convulsive therapy) relieves the symptoms of severe depressive mood disorders, particularly those accompanied by vegetative symptoms. Neuroendocrine abnormalities characterize patients with endogenous depression, and the abnormalities are reversed by convulsive therapy. Tests of neuroendocrine functions provide criteria for the classification of such cases, and probably will be useful in defining suitable cases for convulsive therapy. We postulate that the antidepressant efficacy of convulsive therapy results from the increased release and more widespread cerebral distribution of hypothalamic peptides with behavioral effects. Such a hypothesis provides a basis for clinical trials of centrally active peptides in cases of endogenous depression, and for studies of neuroendocrine functions as predictors of outcome in convulsive therapy.

Adrenocorticotropic Hormone↗
PubMed2006

[Equipment for electro-convulsive therapy].

ECT (electro-convulsive therapy) has been used for the treatment of depressive patients. First it was applied in patients only with sedatives without muscle relaxants, but now we employ muscle relaxants to avoid convulsion and its complications. It is called modified ECT (mECT). General anesthesia using muscle relaxant for ECT is now increasingly employed in Japan. Furthermore, there are some reports that ECT is effective not only in depressive patients but in chronic pain patients. This is why anesthesiologists are especially interested in ECT. In this chapter, clinical application, equipment and complications of ECT are discussed.

Chronic Disease↗
PubMedDate not supplied

The early history of convulsive therapies in Australia.

The early experience of convulsive therapies in Australia was reported in the Medical Journal of Australia from 1935 to 1950. Cardiazol convulsive therapy, first used in Australia in 1937, appears to have been widely employed. Electroconvulsive therapy, first used here in 1941, rapidly became accepted as a mainstream treatment. Early response rates are discussed, as well as Australian adaptations of European techniques. Clinicians of the day considered the use of these procedures carefully and were circumspect about their future role.

Australia↗
PubMedDate not supplied

[Revival of convulsive therapy].

After a brief review of the history of convulsive therapy, the paper criticises the denigratory campaign which was directed against this form of therapy for many years in Italy and later abroad. It stresses that convulsive therapy is now used worldwide, in spite of a few justifiable restrictions, for these indications and that the risks involved in the therapy itself, which are minimum, have been reduced. The Authors complain that this revival, which is now spreading internationally, has been hardly felt in Italy, especially in university circles.

Convulsive Therapy↗
PubMed1991

Metabolic clearance rate of testosterone in male epileptic patients on anti-convulsant therapy.

There are several reports which state that male epileptics on anti-convulsant therapy have reduced sexual activity. We and others have shown that, although total testosterone is raised, the free testosterone concentration is reduced in this patient population. This could be a result of an increased metabolic clearance rate (MCR) of testosterone, inadequate secretion of LH to stimulate testosterone synthesis or inappropriately low testosterone production by the Leydig cells. We have examined these possibilities by measuring the MCR of testosterone in 15 male epileptics on anti-convulsant therapy. In this group of patients, the mean LH (9.3 +/- 5.9 IU/l) and sex-hormone binding globulin (SHBG) (54.5 +/- 22.9 nmol/l) concentrations were significantly greater than those of five normal control subjects (4.7 +/- 1.11 IU/l and 26.0 +/- 7.0 nmol/l respectively). Mean total testosterone concentrations of the two groups were not significantly different but the mean percentage of free testosterone and free testosterone concentration were significantly lower in the patient population (2.06 +/- 0.43 vs 2.98 +/- 0.27 and 0.56 +/- 1.1 vs 0.79 +/- 0.07 pmol/l). The MCR of testosterone was significantly lower in the patients (773 +/- 322 vs 1354 +/- 443 l/day) and showed a positive correlation with the percentage of free testosterone. Therefore, our results suggest that the lowered free testosterone in male epileptics on anti-convulsant therapy is not due to an increased MCR of testosterone. The increased LH concentration suggests primary hypogonadism. This, in turn, could be responsible for low free testosterone levels in the presence of normal testosterone.

Adult↗
PubMed1988

Convulsive Therapy and the Course of Bipolar Illness, 1940-1949.

A total of 93 bipolar patients admitted in the 1940s were divided into those who received convulsive therapy and those who did not. Clinically, the two groups were similar. Those who received convulsive therapy were discharged back home more frequently, indicating the efficacy of the treatment. Those who received convulsive therapy showed more episodes, both manias and depressions, in the course of their illnesses. The reason for this difference in course of illness is not known, but deserves further exploration. The explanation may involve either biological factors or social circumstances related to a successful treatment outcome.

Journal Article↗
PubMed1999

Naturalistic comparative study of outcome and cognitive effects of unmodified electro-convulsive therapy in schizophrenia, mania and severe depression in Nigeria.

BACKGROUND: Although unmodified electro-convulsive therapy (ECT) is widely used in Nigeria for schizophrenia, mania and severe depression failing to respond to adequate pharmacotherapy in the short-term, there are no prospective studies on its efficacy and side effects. OBJECTIVE: To compare the efficacy of electro-convulsive therapy and standard pharmacotherapy in the treatment of schizophrenia, mania and severe depression. DESIGN: A prospective open label study. METHOD: Seventy subjects (mean age, 29.4) with mean duration of illness, 50.6 months, and diagnosis of schizophrenia (37.1%), mania (28.6%), severe depression (30%) and schizo-affective disorder (4.3%), were assessed pre-ECT and at seven other intervals in six months, using the Brief Psychiatric Rating Scale (BPRS), the Mini-Mental State Examination (MMSE) and other cognitive test batteries. They were compared with a matched group of patients who received only pharmacotherapy. RESULTS: Although the ECT group had suffered more treatment resistant disorders, there was full clinical recovery in two months, when all were discharged. The group had significantly shortened duration of hospitalisation, after commencement of ECT. Hence ECT facilitated recovery in this potentially drug treatment resistant psychotic subjects. Although frequency of complaints of subjective memory difficulty increased during ECT and normalised at follow up, objective tests showed steady cognitive improvement with clinical recovery. Complaints of muscle pain (31.4%), post-ECT confusion (15.7%) and post-ECT headache (20%) in the first week of treatment, were not evident at follow up. CONCLUSION: Unmodified ECT combined with pharmacotherapy was safe and effective with non-enduring subjective memory difficulty for this potentially drug treatment resistant group of psychotic patients.

Adolescent↗
PubMed1990

How does convulsive therapy work?

There is no death of hypotheses to explain the antidepressant action of convulsive therapy. Neurohumoral-receptor, kindling-anticonvulsant, and neuroendocrine ideas are prominently discussed. Views based on direct comparisons with antidepressant drugs or based on pharmacologic models are seen as inadequate. The neuroendocrine hypothesis, derived from human studies, appears the most viable. It argues that the affective disorders result from a deficiency of a mood-modifying peptide (antidepressin) derived from the hypothalamus. Convulsive therapy stimulates the production and release of antidepressin. Studies dedicated to the search for this peptide as a replacement for ECT are encouraged.

Adrenocorticotropic Hormone↗