ECT-induced Changes Research Articles

Electroconvulsive Therapy Regulates Brain Connectome Dynamics in Patients With Major Depressive Disorder

BackgroundElectroconvulsive therapy (ECT) is an effective treatment for patients with major depressive disorder (MDD), but its underlying neural mechanisms remain largely unknown. The aim of this study was to identify changes in brain connectome dynamics after ECT in MDD and to explore their associations with treatment outcome. MethodsWe collected longitudinal resting-state functional magnetic resonance imaging data from 80 patients with MDD (50 with suicidal ideation [MDD-SI] and 30 without [MDD-NSI]) before and after ECT and 37 age- and sex-matched healthy control participants. A multilayer network model was used to assess modular switching over time in functional connectomes. Support vector regression was used to assess whether pre-ECT network dynamics could predict treatment response in terms of symptom severity. ResultsAt baseline, patients with MDD had lower global modularity and higher modular variability in functional connectomes than control participants. Network modularity increased and network variability decreased after ECT in patients with MDD, predominantly in the default mode and somatomotor networks. Moreover, ECT was associated with decreased modular variability in the left dorsal anterior cingulate cortex of MDD-SI but not MDD-NSI patients, and pre-ECT modular variability significantly predicted symptom improvement in the MDD-SI group but not in the MDD-NSI group. ConclusionsWe highlight ECT-induced changes in MDD brain network dynamics and their predictive value for treatment outcome, particularly in patients with SI. This study advances our understanding of the neural mechanisms of ECT from a dynamic brain network perspective and suggests potential prognostic biomarkers for predicting ECT efficacy in patients with MDD.

Structural and Functional MRI Brain Changes in Patients with Schizophrenia Following Electroconvulsive Therapy: A Systematic Review.

Schizophrenia (SZ) is a severe psychiatric disorder typically characterized by multidimensional psychotic syndromes. Electroconvulsive therapy (ECT) is a treatment option for medication-resistant patients with SZ or treating acute symptoms. Although the efficacy of ECT has been demonstrated in clinical use, its therapeutic mechanisms in the brain remain elusive. This study aimed to summarize brain changes on structural magnetic resonance imaging (sMRI) and functional MRI (fMRI) after ECT. According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a systematic review was carried out. The PubMed and Medline databases were systematically searched using the following medical subject headings (MeSH): (electroconvulsive therapy OR ECT) AND (schizophrenia) AND (MRI OR fMRI OR DTI OR DWI). This review yielded 12 MRI studies, including 4 with sMRI, 5 with fMRI and 3 with multimodal MRI. Increases in volumes of the hippocampus and its adjacent regions (parahippocampal gyrus and amygdala), as well as the insula and frontotemporal regions, were noted after ECT. fMRI studies found ECT-induced changes in different brain regions/networks, including the hippocampus, amygdala, default model network, salience network and other regions/networks that are thought to highly correlate with the pathophysiologic characteristics of SZ. The results of the correlation between brain changes and symptom remissions are inconsistent. Our review provides evidence supporting ECT-induced brain changes on sMRI and fMRI in SZ and explores the relationship between these changes and symptom remission.

Progressive Changes in Brain Regional Homogeneity Induced by Electroconvulsive Therapy Among Patients With Schizophrenia.

Electroconvulsive therapy (ECT) has significant effects on improving psychotic symptoms in schizophrenia (SZ), but the changes of brain function induced by it are unclear. The purpose of the study was to explore progressive ECT-induced changes in regional homogeneity (ReHo) at multiple time points before, during, and after a course of ECT. The 27 in-patients with SZ (SZ group) who met the recruitment criteria accepted clinical evaluations and resting-state functional magnetic resonance imaging scans before the first ECT (pre-ECT), after the first ECT (ECT1), and after the eighth ECT (ECT8), all conducted within 10 to 12 hours. Forty-three healthy controls (HCs; HC group) who matched well with the patients for age, sex, and years of education were recruited. For Positive and Negative Syndrome Scale (PANSS) and ReHo, progressive changes were examined. Pair-wise comparisons of patient pre-ECT, ECT1, and ECT8 ReHo values with HC ReHo values revealed that ECT normalized the ReHo values in bilateral superior occipital gyrus (SOG), right lingual gyrus (LG), left medial prefrontal cortex. Furthermore, improved ReHo in bilateral SOG and right LG appeared after the first ECT application. The ReHo values in right middle occipital gyrus, right middle temporal gyrus, and right inferior parietal lobule were not significantly altered by ECT. The total PANSS score was lower even after the first ECT application (mean ΔPANSSECT1, 11.7%; range, 2%-32.8%) and markedly reduced after the eighth application (mean ΔPANSSECT8, 86.3%; range, 72.5%-97.9%). The antipsychotic effects of ECT may be achieved through regulating synchronization of some regions such as bilateral SOG, right LG, and left medial prefrontal cortex. Furthermore, the enhanced synchronizations also take place in other regions.

Longitudinal trajectory of response to electroconvulsive therapy associated with transient immune response & white matter alteration post-stimulation.

Research suggests electroconvulsive therapy (ECT) induces an acute neuroinflammatory response and changes in white matter (WM) structural connectivity. However, whether these processes are related, either to each other or to eventual treatment outcomes, has yet to be determined. We examined the relationship between levels of peripheral pro-inflammatory cytokines and diffusion imaging-indexed changes in WM microstructure in individuals with treatment-resistant depression (TRD) who underwent ECT. Forty-two patients were assessed at baseline, after their second ECT (T2), and after completion of ECT (T3). A Montgomery Åsberg Depression Rating Scale improvement of >50% post-ECT defined ECT-responders (n = 19) from non-responders (n = 23). Thirty-four controls were also examined. Tissue-specific fractional anisotropy (FAt) was estimated using diffusion imaging data and the Free-Water method in 17 WM tracts. Inflammatory panels were evaluated from peripheral blood. Cytokines were examined to characterize the association between potential ECT-induced changes in an inflammatory state and WM microstructure. Longitudinal trajectories of both measures were also examined separately for ECT-responders and non-responders. Patients exhibited elevated Interleukin-8 (IL-8) levels at baseline compared to controls. In patients, correlations between IL-8 and FAt changes from baseline to T2 were significant in the positive direction in the right superior longitudinal fasciculus (R-SLF) and right cingulum (R-CB) (psig = 0.003). In these tracts, linear mixed-effects models revealed that trajectories of IL-8 and FAt were significantly positively correlated across all time points in responders, but not non-responders (R-CB-p = .001; R-SLF-p = 0.008). Our results suggest that response to ECT in TRD may be mediated by IL-8 and WM microstructure.

Gradient of electro-convulsive therapy\u2019s antidepressant effects along the longitudinal hippocampal axis

Despite decades of successful treatment of therapy-resistant depression and major scientific advances in the field, our knowledge about electro-convulsive therapy’s (ECT) mechanisms of action is still scarce. Building on strong empirical evidence for ECT-induced hippocampus anatomy changes, we sought to test the hypothesis that ECT has a differential impact along the hippocampus longitudinal axis. We acquired behavioural and brain anatomy magnetic resonance imaging (MRI) data in patients with depressive episode undergoing ECT (n = 9) or pharmacotherapy (n = 24) and healthy controls (n = 30) at two time points 3 months apart. Using whole-brain voxel-based statistical parametric mapping and topographic analysis focused on the hippocampus, we observed ECT-induced gradient of grey matter volume increase along the hippocampal longitudinal axis with predominant impact on its anterior portion. Clinical outcome measures showed strong correlations with both baseline volume and rate of ECT-induced change exclusively for the anterior, but not posterior hippocampus. We interpret our findings confined to the anterior hippocampus and amygdala as additional evidence of the regional specific impact of ECT that unfolds its beneficial effect on depression via the “limbic” system. Main limitations of the study are patients’ polypharmacy, heterogeneity of psychiatric diagnosis, and long-time interval between scans.

Hippocampal volume and memory impairment after electroconvulsive therapy in patients with depression.

Patients hesitate to consent to electroconvulsive therapy (ECT) because of the fear of memory impairment. The mechanisms underlying this impairment are unclear, but several observations suggest hippocampal alterations may be involved. We investigated whether ECT-induced change in hippocampal volume correlates with memory impairment. Using a 3T MRI scanner, we acquired brain images and assessed cognitive performance in 22 severely depressed patients at three time points: (1) before ECT series, (2) within one week after the series, and (3) at six-month follow-up. The hippocampus was segmented into subregions using FreeSurfer. The dentate gyri (DG) were the primary regions of interest (ROIs) and major hippocampal subregions secondary ROIs. Cognitive performance was assessed using the Screen for Cognitive Impairment in Psychiatry and verbal memory using the Verbal Learning subtest. The linear mixed model and the repeated-measures correlation were used for statistical analyses. ECT induced an increase in the right and left DG volume with co-occurring worsening in verbal memory, and these changes were within-patients negatively correlated (right DG, rrm =-0.85, df=18, p=0.0000002; left DG, rrm =-0.58, df=18, p=0.008). At a six-month follow-up, the volume of both DG decreased with a co-occurring improvement in verbal memory, and these changes were negatively correlated in the right DG (rrm =-0.64, df=15, p=0.005). Volume increases in 14 secondary ROIs were also negatively correlated with memory impairment. ECT-related transient increases in the volume of major hippocampal subregions within-patients are associated with memory impairment. Hippocampal alterations following ECT should be the focus in searching for causes of the cognitive side effects.

Anterior cingulate gamma-aminobutyric acid concentrations and electroconvulsive therapy.

ObjectiveThe anticonvulsant hypothesis posits that ECT’s mechanism of action is related to enhancement of endogenous anticonvulsant brain mechanisms. Results of prior studies investigating the role of the inhibitory neurotransmitter gamma‐aminobutyric acid (“GABA+”, GABA and coedited macromolecules) in the pathophysiology and treatment of depression remain inconclusive. The aim of our study was to investigate treatment‐responsive changes of GABA+ in subjects with a depressive episode receiving electroconvulsive therapy (ECT).MethodsIn total, 41 depressed subjects (DEP) and 35 healthy controls (HC) were recruited at two independent sites in Norway and the USA. MEGA‐PRESS was used for investigation of GABA+ in the anterior cingulate cortex. We assessed longitudinal and cross‐sectional differences between DEP and HC, as well as the relationship between GABA+ change and change in depression severity and number of ECTs. We also assessed longitudinal differences in cognitive performance and GABA+ levels.ResultsDepressive episode did not show a difference in GABA+ relative to HC (t 71 = −0.36, p = .72) or in longitudinal analysis (t 36 = 0.97, p = .34). Remitters and nonremitters did not show longitudinal (t 36 = 1.12, p = .27) or cross‐sectional differences in GABA+. GABA+ levels were not related to changes in antidepressant response (t 35 = 1.12, p = .27) or treatment number (t 36 = 0.05, p = .96). An association between cognitive performance and GABA+ levels was found in DEP that completed cognitive effortful testing (t 18 = 2.4, p = .03).ConclusionOur results failed to support GABA as a marker for depression and abnormal mood state and provide no support for the anticonvulsant hypothesis of ECT. ECT‐induced change in GABA concentrations may be related to change in cognitive function.

Neuronal network mechanisms associated with depressive symptom improvement following electroconvulsive therapy.

Electroconvulsive therapy (ECT) is the most effective antidepressant treatment for severe depression. Although recent structural magnetic resonance imaging (MRI) studies have consistently reported ECT-induced hippocampal volume increases, most studies did not find the association of the hippocampal volume changes with clinical improvement. To understand the underlying mechanisms of ECT action, we aimed to identify the longitudinal effects of ECT on hippocampal functional connectivity (FC) and their associations with clinical improvement. Resting-state functional MRI was acquired before and after bilateral ECT in 27 depressed individuals. A priori hippocampal seed-based FC analysis and a data-driven multivoxel pattern analysis (MVPA) were conducted to investigate FC changes associated with clinical improvement. The statistical threshold was set at cluster-level false discovery rate-corrected p < 0.05. Depressive symptom improvement after ECT was positively associated with the change in the right hippocampus-ventromedial prefrontal cortex FC, and negatively associated with the right hippocampus-superior frontal gyrus FC. MVPA confirmed the results of hippocampal seed-based analyses and identified the following additional clusters associated with clinical improvement following ECT: the thalamus, the sensorimotor cortex, and the precuneus. ECT-induced change in the right frontotemporal connectivity and thalamocortical connectivity, and changes in the nodes of the default mode network were associated with clinical improvement. Modulation of these networks may explain the underlying mechanisms by which ECT exert its potent and rapid antidepressant effect.

Association between hippocampal volume change and change in memory following electroconvulsive therapy in late-life depression.

Electroconvulsive therapy (ECT)-induced hippocampal volume change (HVC) has been repeatedly described in recent years. The similar time course of HVC and ECT-related cognitive effects suggest a relation, that is to date, understudied. This study investigates whether HVC following ECT predicts the change in memory performance six months after the end of the ECT treatment. Hippocampal volume (HV) was measured via high-resolution 3D T1-weighted images in 88 patients with late-life depression, within 1week before and after ECT. Memory performance was assessed before and six months after ECT. Multiple linear regression was used to examine whether change in memory performance could be predicted based on ECT-induced changes in HV. Larger right absolute HVC predicts less pronounced improvement on the VAT (visual memory) in the whole sample. For the 8-Word Test (verbal memory), Category Fluency Test (semantic memory), and MMSE, the effect is only present in patients who switched from right unilateral to bitemporal stimulation after six ECT sessions. Absolute HVC in the left hemisphere was not significantly related to cognitive change. A larger absolute change in right HV during ECT is associated with less improvement in memory performance up to 6months post-ECT.

Cortisol is not associated with pre-treatment medial temporal lobe volume or volume changes after electroconvulsive therapy in patients with late-life depression

Accumulating evidence suggests that late-life depression is associated with reduced hippocampal volume and that cortisol might be related to this volumetric reduction. We explored whether cortisol awaking response (CAR), which is the increase in cortisol after awakening, was associated with volumetric changes in the medial temporal lobe (MTL) after electroconvulsive therapy (ECT) in 41 patients (age ≥ 55) treated for major depressive disorder (MDD) with ECT. Cortisol was measured before the start of the ECT treatment and was related to MTL volumes derived from structural T1-weighted images. The study assessed associations between CAR and pre-treatment MTL volumes, and CAR and ECT-induced MTL volumetric changes. There were no significant correlations found between CAR, operationalized as Area Under the Curve with respect to ground (AUCg) and Area Under the Curve with respect to increase (AUCi), and pre-treatment MTL volumes. Neither was there an association between AUCg or AUCi and the ECT-induced changes in MTL volumes after correction for multiple comparisons. Finally, neither AUCg or AUCi were able to predict ECT-induced volumetric changes in the MTL. Hence, we conclude that CAR is unrelated to pre-treatment hippocampus and amygdala volumes, and to the volumetric changes in the aforementioned areas following ECT.

The Principles of Electroconvulsive Therapy Based on Correlations of Schizophrenia and Epilepsy: A View From Brain Networks.

Electroconvulsive therapy (ECT) was established based on Meduna's hypothesis that there is an antagonism between schizophrenia and epilepsy, and that the induction of a seizure could alleviate the symptoms of schizophrenia. However, subsequent investigations of the mechanisms of ECT have largely ignored this originally established relationship between these two disorders. With the development of functional magnetic resonance imaging (fMRI), brain-network studies have demonstrated that schizophrenia and epilepsy share common dysfunctions in the default-mode network (DMN), saliency network (SN), dorsal-attention network (DAN), and central-executive network (CEN). Additionally, fMRI-defined brain networks have also been shown to be useful in the evaluation of the treatment efficacy of ECT. Here, we compared the ECT-induced changes in the pathological conditions between schizophrenia and epilepsy in order to offer further insight as to whether the mechanisms of ECT are truly based on antagonistic and/or affinitive relationships between these two disorders.

Inter and intra-hemispheric structural imaging markers predict depression relapse after electroconvulsive therapy: a multisite study

Relapse of depression following treatment is high. Biomarkers predictive of an individual’s relapse risk could provide earlier opportunities for prevention. Since electroconvulsive therapy (ECT) elicits robust and rapidly acting antidepressant effects, but has a >50% relapse rate, ECT presents a valuable model for determining predictors of relapse-risk. Although previous studies have associated ECT-induced changes in brain morphometry with clinical response, longer-term outcomes have not been addressed. Using structural imaging data from 42 ECT-responsive patients obtained prior to and directly following an ECT treatment index series at two independent sites (UCLA: n = 17, age = 45.41±12.34 years; UNM: n = 25; age = 65.00±8.44), here we test relapse prediction within 6-months post-ECT. Random forests were used to predict subsequent relapse using singular and ratios of intra and inter-hemispheric structural imaging measures and clinical variables from pre-, post-, and pre-to-post ECT. Relapse risk was determined as a function of feature variation. Relapse was well-predicted both within site and when cohorts were pooled where top-performing models yielded balanced accuracies of 71–78%. Top predictors included cingulate isthmus asymmetry, pallidal asymmetry, the ratio of the paracentral to precentral cortical thickness and the ratio of lateral occipital to pericalcarine cortical thickness. Pooling cohorts and predicting relapse from post-treatment measures provided the best classification performances. However, classifiers trained on each age-disparate cohort were less informative for prediction in the held-out cohort. Post-treatment structural neuroimaging measures and the ratios of connected regions commonly implicated in depression pathophysiology are informative of relapse risk. Structural imaging measures may have utility for devising more personalized preventative medicine approaches.

Serum tryptase level and inflammatory markers in exhaled breath condensate of children with exercise-induced symptoms.

The pathogenesis of exercise-induced bronchoconstriction (EIB) is poorly understood. To evaluate the biomarkers concentration in exhaled breath condensate (EBC) in schoolchildren with postexercise symptoms. We also evaluated changes in fractional exhaled nitric oxide (FeNO) value and the serum tryptase level after exercise. One hundred children with postexercise symptoms were included. Methacholine challenge testing (MCT) was performed at visit 2, and exercise challenge testing (ECT) was performed at visit 3. Before and after ECT serum tryptase levels and FeNO values were measured. EBC was collected after ECT from 10 randomly selected children from each group. The children were assigned to the following groups: ECT(+) MCT(+), ECT(+) MCT(-), ECT(-) MCT(+), ECT(-) MC(-). We measured the following molecules: eotaxin, interleukin (IL) 8, IL-1ra, IL-1 beta, IL-6, IL-1 alpha, IL-12(p40), IL-5, granulocyte-macrophage colony-stimulating factor, IL-7, IL-15, IL-4, IL-2, IL-10, tumor necrosis factor alpha, interferon gamma, IL-13, tumor necrosis factor beta, monocyte chemoattractant protein-1, IL-17A, macrophage inflammatory proteins-1 alpha, macrophage inflammatory proteins-1 beta, IL-12(p70), and regulated on activation, normal T-cell expressed and secreted by using a multiplex immunoassay. Prostaglandin E2 (PGE2), leukotriene B4, and cysteinyl leukotriene were analyzed by using separate enzyme-linked immunosorbent assay kits. In the MCT(+) group, a detectable level of IL4 in EBC and detectible levels of eicosanoids were seen in the ECT(+) group. We observed the opposite direction of ECT-induced changes in FeNO and serum tryptase concentrations in patients with detectable compared with patients without detectable levels of cytokines in EBC. We showed ECT-induced reduction in the tryptase level in patients with a nondetectable PGE2 level in EBC and an increase in tryptase levels in patients who had detectable levels of PGE2 in EBC. EBC was a useful method to estimate inflammation but only in children with symptoms and with EIB shown by a positive ECT. Children with a positive ECT had detectable levels of eicosanoids in EBC; the opposite direction of ECT-induced changes in FeNO and serum tryptase concentrations was observed. The results of above study confirm the role of mast cells and eicosanoids in the pathogenesis of EIB in children.

Autobiographical Memory Specificity in Major Depression Treated With Electroconvulsive Therapy.

Autobiographical memory in major depression is characterized by reduced specificity, which reflects the tendency to summarize categories of events rather than recall specific instances of events situated in a time and place. This widely studied cognitive marker for depression has not been extensively examined in patients treated with electroconvulsive therapy (ECT). We conducted a retrospective chart review of a naturalistic cohort of patients receiving a course of brief-pulse predominantly bitemporal ECT for a major depressive episode. Patients completed the recent life section of the Kopelman Autobiographical Memory Interview (AMI) at pre-ECT baseline, end of treatment course, and 3-month follow-up as part of routine clinical practice. Mood was assessed using the 24-item Hamilton Rating Scale for Depression. We identified 48 patients (mean age, 61.6; female, 62.5%) meeting inclusion criteria. A total of 77.1% of patients responded to the ECT course, 29.7% subsequently relapsed. There were no significant changes over time on either AMI total score or semantic and episodic subscales. However, patients were markedly impaired on episodic autobiographical memory compared with the normative sample at all 3 assessment points, whereas personal semantic memory recall was normal. Specificity of episodic autobiographical memory at baseline did not predict response to ECT or likelihood of relapse. We found reduced specificity of episodic autobiographical memory in depressed patients before ECT, which persisted at long-term follow-up despite significant improvement in mood. The finding of no detectable retrograde amnesia likely reflects lack of sensitivity of the recent life section of the AMI to detect ECT-induced changes.

The Immune System and Electroconvulsive Therapy for Depression

Electroconvulsive therapy (ECT) remains the most effective and fast-acting treatment option for several psychiatric conditions, including treatment-resistant depression. Although ECT has been in use for 75 years, the mechanism of action is unknown. There is emerging evidence that modulation of the hypothalamic-pituitary-adrenal axis may mediate, in part, the therapeutic action of ECT. A growing body of evidence points to links between disturbances in the immune system and depression. However, the impact of ECT on immune functioning and the possible role of alterations in the immune system as a mechanism of action of ECT remain elusive. To provide a literature overview on the effects of ECT on the immune system. Relevant articles and abstracts in English were retrieved from PubMed/Medline using search terms related to ECT, inflammation, and immune system. The results of studies examining ECT-induced changes in immune functioning as well as the degree to which these represent possible mechanisms mediating the therapeutic action of ECT were summarized. Our search identified only a limited number of studies. The findings suggest that a single session of ECT induces an acute, transient immune activation, whereas repetitive ECT treatment results in long-term down-regulation of immune activation. However, inconsistency in findings and methodological issues, including sample size and lack of consideration of confounding factors affecting cytokine concentrations, precludes definitive conclusion. To elucidate the possible role of immunological changes mediating the effect of ECT, more prospective controlled studies with larger sample sizes are required.

Mechanism Underlying the Therapeutic Effects of Electroconvulsive Therapy (ECT) on Depression

Electroconvulsive therapy (ECT) is used to treat drug-resistant depressive disorders. The results of studies on the mechanism underlying the effectiveness of ECT on depression are still controversial. ECT stimulus is usually larger than the threshold of induction of seizures and activation of whole-brain is believed to be necessary to produce therapeutic effects. A single ECT session induces alterations of the electroencephalogram (EEG) including initial epileptic discharges, then slow waves, and finally flattened EEG. Repeated ECT results in an increasing number of slower waves in the EEG for as long as a month. ECT-induced changes in various neurotransmitter systems have also been reported. Serotonin (5-hydroxytryptamine, 5-HT) is one of the most important neurotransmitters involved in depressive illness, and ECT alters several 5-HT-receptor subtypes in the central nervous system. 5-HT1A receptors in post-synaptic neurons are sensitized by repeated ECT, but those in pre-synaptic neurons (auto-receptors) are not changed. In addition, our electrophysiological studies have shown that ECT increases sensitivity to 5-HT of 5-HT3 receptors in the hippocampus, resulting in an increase in release of neurotransmitters such as glutamate and γ-aminobutyric acid. In contrast, ECT decreases the auto-receptor functions in noradrenergic and dopaminergic neurons in the locus coeruleus and substantia nigra, respectively, resulting in an increase in release of noradrenaline and dopamine. In conclusion, 5-HT1A-receptor sensitization may be important for explaining the effectiveness of ECT, as this change induces a decrease in the number of 5-HT2A receptors that are elevated in depressive patients. Facilitation of neurotransmitter releases due to 5-HT3-receptor sensitization by ECT may also play an important role in effective treatment of depressive patients refractory to therapeutic drugs.

Effects of acute and chronic electroconvulsive treatment on interstitial concentrations of somatostatin in the rat hippocampus and striatum

1. 1. Effects of acute and chronic electroconvulsive treatment (ECT) and sham-ECT on extracellular concentrations of somatostatin-like immunoreactivity (SS-LI) from the hippocampus and striatum of awake rats were studied with in vivo microdialysis in combination with a high-sensitivity radioimmunoassay. 2. 2. Acute ECT and sham-ECT did not affect hippocampal or striatal SS-LI concentrations during the first 4 hr after the treatment. However, 24 hr later acute ECT significantly decreased SS-LI concentrations from both areas by approximately 40%. 3. 3. Chronic ECT and sham-ECT did not influence basal hippocampal or striatal SS-LI concentrations. 4. 4. Administration of a challenge ECT in animals treated chronically with ECT or sham-ECT did not affect hippocampal or striatal SS-LI concentrations during the first 4 hr after the treatment. However, 24 hr later hippocampal and striatal SS-LI levels were decreased by 30–40% in all groups. 5. 5. The delayed ECT-induced changes in regional, extracellular concentrations of SS-LI may be secondary to increased somatostatin metabolism and are perhaps related to the therapeutic or adverse effects of this antidepressant treatment.

Plasma pattern of adrenocorticotropin and cortisol during electroconvulsive therapy in patients with major depressive illness.

Thirty-three patients with major depressive illness were treated with electroconvulsive therapy (ECT) and plasma adrenocorticotropin (ACTH), and cortisol levels were measured 30 min before and 1, 5, 15, 30 and 60 min after ECT. There was an immediate release of ACTH with a maximum after 5 min. The maximum cortisol plasma levels were measured 30 min after ECT. No change in ACTH and cortisol concentrations was seen in control experiments when the patients received only anaesthesia. ACTH release was seen in patients treated with ECT in the morning and in the evening. In 15 patients the levels were studied at the first and sixth (last) ECT. ACTH and cortisol levels were significantly higher after the first ECT as compared with the sixth. This alteration in ACTH release might reflect ECT-induced changes in the central monoaminergic transmission with stimulation of beta-adrenergic pathways leading to inhibition of ACTH-release.

Improvement of Parkinsonism in depressed patients treated with ECT.

Two patients with severe Parkinson's disease were treated with electroconvulsive therapy for a supervening depression. Not only did the symptoms of depression clear up after only four treatments, but the parkinsonian signs also showed striking and sustained improvement. This may be related to ECT-induced changes in dopamine and norepinephrine metabolism. Parkinsonism does not appear to be a contraindication to ECT. On the contrary, ECT may be the treatment of choice for certain patients with Parkinson's disease, whether nor not it is complicated by intractable depression.