[Comparative study of spinal fractures in electric acupuncture convulsive therapy, electric convulsive therapy and epilepsy].
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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.
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.
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.
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.
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.
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.
The therapeutic effect of simulated and real bilateral electric convulsion therapy was examined in a double-blind, randomised trial on 22 patients with a primary depressive illness. Each treatment was given twice weekly for three weeks and the results assessed by the psychiatrist using a visual analogue rating scale, nurses using a nine-point rating scale, and the patients themselves using the Beck Depression Inventory. With all three methods of assessment patients given the real treatment substantially improved (p less than 0.001), whereas those given simulated treatment showed little change. Three weeks after substituting real treatment for simulated, however, these patients were also significantly improved (psychiatrist's rating p less than 0.001; nurses' rating p less than 0.005; Beck inventory p less than 0.005). These findings confirm the value of electric convulsion therapy in severe depressive illness and strongly suggest that the convulsion is important for the therapeutic effect.
The influence of age and number of treatments on memory impairment was studied in depressed patients after a series of convulsive treatments: bilateral ECT, unilateral ECT on the nondominant hemisphere, and fluorothyl convulsive therapy. Before and after the completed convulsive therapy course the patients were tested with a memory test battery and the symptoms rated with a depression scale. Before treatment older age-groups had decreased ability to learn, but their post-treatment forgetting score was not significantly higher than in other age-groups. An increase in the number of ECTs did not seem to correlate with the degree of memory impairment. The conclusion of the present study is that age (up to 65) and the number of ECTs (up to 10) have no apparent influence on memory impairment after electroconvulsive therapy.
The authors, drawing from their very large experience, describe technics of administering anesthesia and muscle-relaxing agents for convulsive therapy. After a brief historical review, they mention in detail the materials used and the set up for this modified electroconvulsive treatment. They describe the signs of amnesia and those of muscular relaxation in order to administer a modified electroconvulsive treatment properly. A comparison of this modification with various other methods used in different centers is made. A section of the paper is devoted to the less common use of Indoklon. Contraindications for the various therapeutic methods are mentioned and a critical evaluation is provided. The authors draw conclusions from their clinical experience and give the results of their observations. The management of various side-effects and possible complications is discussed. The article should be considered as a guide in the use of modified convulsive therapy.
Results of ammonium convulsive therapy (ACT) in 203 patients with neurotic depressive states of various nosological origin are presented. In the total population subjected to 4-20 sessions of ACT, a full recovery or a good remission were attained in 89% of patients. The remission starts after 2 to 4 sessions with the improvement of basic mood and reducing of anxiety. Later continuous activation of the behavior may be seen. The best results were attained in patients with depressive, hypochondriac and neurasthenic neuroses, especially when astheno-, anxious-depressive or astheno-hypochondriac syndromes predominated. ACT is well tolerated by patients with no marked side effects. ACT can be recommended as a safe and effective treatment method in patients with moderate depression.
Since the introduction of seizures as a therapy in psychiatry in 1934, much has been learned about the target populations, modes of induction, means to make the treatment safer, and the mechanisms underlying the therapeutic process. The repeated and spaced induction of seizures relieves the symptoms of severe depressive psychoses. The presence of vegetative symptoms is a predictor of good outcome, and brain stem stimulation is a feature of successful treatment. The safest inductions are those using barbiturate and succinylcholine anesthesia, hyperoxygenation, unilateral electrode placements, and minimal inducing currents. Patients with severe depression present neuroendocrine abnormalities, which return to normal with convulsive therapy. Recently, peptides of hypothalamic origin have been identified which have behavioural and mood altering effects. From these experiences, we suggest that the antidepressant efficacy of convulsive therapy results from the increased release and greater penetration into the brain of hypothalamic peptides with behavioral effects.
Electric convulsion therapy (E.C.T.) was used in the treatment of 13 women inpatients suffering from depressive symptoms. Twelve of the patients showed a significant increase in urinary excretion of 3', 5' cyclic adenosine monophosphate (cAMP) on the day of treatment, whereas four controls who received all or part of the preliminary treatment but no electric shock showed a reduction. The results of this study are consistent with the hypothesis that the antidepressant action of E.C.T. is mediated through an increased production of cAMP in brain tissue.
Recent legislation in NSW betrays a prejudice against electro-convulsive therapy. Factors probably contributing to popular prejudice against ECT are discussed.
Although there is still considerable controversy surrounding electro-convulsive therapy (ECT), it is widely used in psychiatric hospitals. Good nursing care is central to its successful administration, and nurses must be able to explain the procedure to patients and why it can help them.
We reviewed all documented cases of spontaneous seizures that followed convulsive therapy. Nineteen studies provided information in 81 cases. The average annual incidence of spontaneous seizures was 114 per 100,000, 5 times more frequent than an age-adjusted nonpsychiatric cohort. Host susceptibility rather than treatment features influenced seizure development. A longer latency to first seizure was associated with greater likelihood of seizure recurrence, a relationship also observed in posttraumatic epilepsy.
The ability of electrically-induced convulsions to alleviate at least some symptoms of mental illness was first reported in the literature 50 years ago; however, the cerebral mechanisms responsible for such therapeutic effects have thus far escaped elucidation. It is thus interesting to note that those seeking explanations for the therapeutic effects of electroconvulsive therapy (ECT) have focused their attention on the convulsion produced by ECT, as opposed to the coma. The present hypothesis emphasizes the coma following the convulsion as a potential explanation of the effectiveness of ECT and other convulsive therapies. It is postulated that the primary effect of the convulsion is to cause the release of adenosine (ARN) from neuronal tissue and that the subsequent depressant effect of ARN on neuronal activity results in the clinical effect observed. Thus hypothesis suggests that chemically-induced coma, particularly coma induced by benzodiazepines, may offer a safe, effective and more acceptable alternative to ECT.
A survey by questionnaire of all senior psychiatrists in the Wessex Region showed that they considered depressive psychosis to be the major indication for electric convulsion therapy (ECT). A good clinical response was thought to be predicted by the presence of psychomotor retardation, depressive delusions, depressed mood, early morning wakening, diurnal variation, loss of appetite, and agitation. ECT was judged to be extremely useful for treating mania and acute undifferentiated, catatonic, and paranoid schizophrenia; of some use in hypochondriasis; but of little value or contraindicated when there was severe, depersonalisation, or hysterical symptoms. Only 40% of the psychiatrists favoured unilateral ECT, and the variation in electrode placements used by different psychiatrists was surprising. Eighty per cent of the respondents used courses averaging six to eight treatments given over two or three weeks. Results obtained in this study, based on clinical judgment, differed from research findings, which emphasises the need for further study of this important treatment.