How Does Electroconvulsive Therapy Work? Theories on its Mechanism

Bolwig, Tom G.

doi:10.1177/070674371105600104

Cited by 137 publications

(94 citation statements)

References 55 publications

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“…It proposes that seizure activity in the limbic system induces neurotrophic effects crucial for therapeutic efficacy (Bolwig, 2011). This hypothesis is in line with the preclinically developed notion that stress is associated with neuronal atrophy and reduced neurogenesis (Duman and Aghajanian, 2012), impaired synaptic plasticity, and dendritic arborization in the hippocampus (Sousa et al, 2000), whereas antidepressants and electroconvulsive stimulation (ECS; the animal model of ECT) stimulate neurogenesis (Bolwig, 2011), synaptogenesis, gliogenesis, and angiogenesis (Duman and Aghajanian, 2012;Bouckaert et al, 2014).…”

Section: Introductionmentioning

confidence: 63%

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Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Bouckaert

Dols

Emsell

et al. 2016

Neuropsychopharmacol

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Recent structural imaging studies have described hippocampal volume changes following electroconvulsive therapy (ECT). It has been proposed that serum brain-derived neurotrophic factor (sBDNF)-mediated neuroplasticity contributes critically to brain changes following antidepressant treatment. To date no studies have investigated the relationship between changes in hippocampal volume, mood, and sBDNF following ECT. Here, we combine these measurements in a longitudinal study of severe late-life unipolar depression (LLD). We treated 88 elderly patients with severe LLD twice weekly until remission (Montgomery-Åsberg Depression Rating Scale (MADRS) o10). sBDNF and MADRS were obtained before ECT (T0), after the sixth ECT (T1), 1 week after the last ECT (T2), 4 weeks after the last ECT (T3), and 6 months after the last ECT (T4). Hippocampal volumes were quantified by manual segmentation of 3T structural magnetic resonance images in 66 patients at T0 and T2 and in 23 patients at T0, T2, and T4. Linear mixed models (LMM) were used to examine the evolution of MADRS, sBDNF, and hippocampal volume over time. Following ECT, there was a significant decrease in MADRS scores and a significant increase in hippocampal volume. Hippocampal volume decreased back to baseline values at T4. Compared with T0, sBDNF levels remained unchanged at T1, T2, and T3. There was no coevolution between changes in MADRS scores, hippocampal volume, and sBDNF. Hippocampal volume increase following ECT is an independent neurobiological effect unrelated to sBDNF and depressive symptomatology, suggesting a complex mechanism of action of ECT in LLD.

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Section: Introductionmentioning

confidence: 63%

“…The 'anatomical-ictal hypothesis' (Bolwig, 2011) aims to unify the concepts introduced above by relating hippocampal dysfunction and neuroplasticity to the working mechanism of ECT. It proposes that seizure activity in the limbic system induces neurotrophic effects crucial for therapeutic efficacy (Bolwig, 2011).…”

Section: Introductionmentioning

confidence: 99%

Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Bouckaert

Dols

Emsell

et al. 2016

Neuropsychopharmacol

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“…Since the introduction of the modified ECT procedure, the risk of fractures has decreased, and these are very rare today (12). Several brain areas are believed to be important for the mode of action of ECT, and different theories behind the antidepressant effect have emerged over the years [for review see (13)]. For example, it has been demonstrated that sub-convulsive seizures have inadequate antidepressant effect and that seizures need to be fully generalised in order to be effective (14).…”

Section: Introductionmentioning

confidence: 99%

Systematic evaluation of skeletal fractures caused by induction of electroconvulsive seizures in rat state a need for attention and refinement of the procedure

Ekemohn

Nielsen

Grahm

et al. 2017

Acta Neuropsychiatr.

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Ekemohn M, Kjaer Nielsen M, Grahm M, Tingström A, Kousholt B, Wegener G, Bay-Richter C. Systematic evaluation of skeletal fractures caused by induction of electroconvulsive seizures in rat state a need for attention and refinement of the procedure.Objective: Electroconvulsive therapy (ECT) is one of the most efficient treatments for major depression. Electroconvulsive seizures (ECS), the animal model of ECT, is widely used to study both mechanisms of action and adverse effects of ECT. As the treatment itself serves as an instant anaesthetic and anaesthetic agents may affect memory functions and behaviour, ECS is traditionally administered without muscle relaxation and anaesthesia. A major problem of unmodified ECS, which has only been addressed peripherally in the literature, is that some animals sustain spinal fractures and subsequent hind leg paralysis (paraplegia). This phenomenon leads to a higher degree of suffering and these animals need to be excluded from the studies. To reach sufficient statistical power, the group sizes are therefore often increased and this may lead to a pre-selected study group in risk of skewing the results. Moreover, the study design of the experiments do not comply with the 3R principles, which advocate for both refinement and reduction of animal experiments. The objective of this study is to systematically evaluate injuries caused by ECS. Methods: We summarise the incidence of spinal fractures from 24 studies conducted during 2009-2015 in six different rat strains and report preliminary findings on scapular fractures following auricular ECS. Results: In total, 12.8% of all tested animals suffered from spinal fractures and we find an increase in spinal fracture incidence over time. Furthermore, X-ray analyses revealed that some animals displayed scapular fractures. Conclusion: We discuss consequences of and possible explanations for ECS-induced fractures. Modifications of the method are highly warranted and we furthermore suggest that all animals are thoroughly examined for discrete fractures. Significant outcomes• In total, 12.8% of all tested animals suffered from spinal fractures.• Spinal fracture incidence increased over time.

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“…This multimodal mechanism of action might be one explanation for the varied clinical effects of ECT in very different clinical syndromes, such as severe depression and manic psychosis. It might also explain the huge variety of neurobiological changes that have been found in studies of ECT, ranging from enhancing serotonergic transmission and activating the mesocorticolimbic dopamine system, affecting the glutamate to GABA balance, restoring neuroendocrine function (reversal of HPA axis derangement) and changing functional activity in different brain regions (Swartz 2009, Bolwig 2011). The provoked seizure results in a sudden, endogenous initiated, cerebral activity inhibition, which then ends the seizure (ictal suppression).…”

Section: The Neurobiological Understanding Of Ectmentioning

confidence: 99%

On electroconvulsive therapy in depression : Clinical, cognitive and neurobiological aspects

Nordanskog¹

2015

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Electroconvulsive therapy (ECT) is used worldwide to treat severe mental disorders. The most common mental disorder, and the third leading cause of disease burden in the world is depression. The clinical efficacy of ECT for severe depression is well-established. However, both the pathophysiology of depression and the mechanism of action of ECT remain elusive. The main aims of this thesis are to address the following issues: 1) the use and practice of ECT in Sweden has not been systematically evaluated since 1975, 2) cognitive side-effects (memory disturbances) are a major concern with ECT and 3) the mechanism of action of ECT remain elusive. The neurobiological aspects of ECT focus on two hypotheses. First, the recent years´ preclinical studies that have provided evidence that ECT induces hippocampal cell proliferation, including neurogenesis. Second, that enhanced functional inhibition of neuronal activity is a key feature. Current use and practice of ECT in Sweden (paper I) is based on data from the national quality register for ECT, the mandatory patient register of the National Board of Health and Welfare and a survey. Treated person rate (TPR) in Sweden 2013 was found to be 41 individuals / 100 000, and thus unchanged since the latest systematic investigation in Sweden 1975. In more than 70% of treatment series the indication was a depressive episode. The selection of patients for ECT and treatment technique in Sweden was similar to that in other western countries, but the consent procedure and the involvement of nurses and nursing assistants in the delivery of ECT differ. Data also shows that there is room for improvement in both the specificity of use and availability of ECT. The second study in this thesis is a longitudinal observational trial where 12 (paper II and III) and 14 (paper IV) patients with depression referred for ECT were investigated. Patients underwent a 3 T MRI structural scanning and DSC-MRI perfusion, a neuropsychological test battery and clinical ratings before ECT, within one to two weeks after ECT and after 6 and 12 months. In line with preclinical findings and the plasticity hypothesis of mechanism of action of ECT, the hippocampal volume increased after ECT in patients with depression. However, this increase was transient and returned to baseline levels within 6 months. No correlation was found between volumetric changes and clinical effect or cognitive outcome. Instead our results suggested an association to the number of treatments, without relation to the side of stimulation. A right-sided decrease in frontal blood flow distinguished remission from non-remission after ECT. There were significant impairments in verbal episodic memory and verbal fluency within one week after ending the ECT course, but these impairments were transient and no persistent cognitive impairments were seen during the follow-up. In summary, this thesis present the first update on the use and practice of ECT in Sweden in the last 40 years as well as a pioneering MRI-study on the hippocampal volume increase...

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How Does Electroconvulsive Therapy Work? Theories on its Mechanism

Cited by 137 publications

References 55 publications

Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Relationship Between Hippocampal Volume, Serum BDNF, and Depression Severity Following Electroconvulsive Therapy in Late-Life Depression

Systematic evaluation of skeletal fractures caused by induction of electroconvulsive seizures in rat state a need for attention and refinement of the procedure

On electroconvulsive therapy in depression : Clinical, cognitive and neurobiological aspects

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