CSF monoamine metabolites and neuropeptides in depressed patients before and after electroconvulsive therapy

2008 ◽  
Vol 23 (5) ◽  
pp. 356-359 ◽  
Author(s):  
Georg Nikisch ◽  
Aleksander A. Mathé
Keyword(s):  
Electroconvulsive Therapy ◽  
Antidepressant Treatment ◽  
Antidepressant Drugs ◽  
Treatment Modalities ◽  
Depressed Patients ◽  
Human Cerebrospinal Fluid ◽  
Rodent Brain ◽  
Before And After ◽  
Hydroxyindoleacetic Acid ◽  
The Common

AbstractAntidepressant drugs affect monoamines and neuropeptides in human cerebrospinal fluid (CSF) and in rodent brain. The purpose of this study was to investigate if also electroconvulsive therapy (ECT) affects these compounds in a similar manner in the CSF of depressed patients. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and corticotropin-releasing hormone (CRH)-like immunoreactivity (-LI) and neuropeptide Y (NPY)-LI were determined in CSF in six drug resistant patients with major depression. Lumbar puncture was performed at baseline and after completion of eight ECTs. ECT was associated with an increase in NPY-LI (p = 0.009) and a decrease in CRH-LI (p ≤ 0.001). HVA (p = 0.003) and 5-HIAA (p = 0.002) were significantly increased after the ECT. Findings of NPY increase and CRH decrease were similar to those following chronic treatment with citalopram, indicating that these changes might constitute one of the common underpinnings of antidepressant treatment modalities.

scholarly journals Methylome-wide change associated with response to electroconvulsive therapy in depressed patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lea Sirignano ◽  
Josef Frank ◽  
Laura Kranaster ◽  
Stephanie H. Witt ◽  
Fabian Streit ◽  
...  
Keyword(s):  
Electroconvulsive Therapy ◽  
Rating Scale ◽  
Antidepressant Treatment ◽  
Cpg Sites ◽  
Cpg Site ◽  
Depressed Patients ◽  
Resistant Depression ◽  
Functional Pathway ◽  
Regional Analyses ◽  
The Relationship

AbstractElectroconvulsive therapy (ECT) is a quick-acting and powerful antidepressant treatment considered to be effective in treating severe and pharmacotherapy-resistant forms of depression. Recent studies have suggested that epigenetic mechanisms can mediate treatment response and investigations about the relationship between the effects of ECT and DNA methylation have so far largely taken candidate approaches. In the present study, we examined the effects of ECT on the methylome associated with response in depressed patients (n = 34), testing for differentially methylated CpG sites before the first and after the last ECT treatment. We identified one differentially methylated CpG site associated with the effect of ECT response (defined as >50% decrease in Hamilton Depression Rating Scale score, HDRS), TNKS (q < 0.05; p = 7.15 × 10−8). When defining response continuously (ΔHDRS), the top suggestive differentially methylated CpG site was in FKBP5 (p = 3.94 × 10−7). Regional analyses identified two differentially methylated regions on chromosomes 8 (Šídák’s p = 0.0031) and 20 (Šídák’s p = 4.2 × 10−5) associated with ΔHDRS. Functional pathway analysis did not identify any significant pathways. A confirmatory look at candidates previously proposed to be involved in ECT mechanisms found CpG sites associated with response only at the nominally significant level (p < 0.05). Despite the limited sample size, the present study was able to identify epigenetic change associated with ECT response suggesting that this approach, especially when involving larger samples, has the potential to inform the study of mechanisms involved in ECT and severe and treatment-resistant depression.

scholarly journals Nonpharmacological, somatic treatments of depression: electroconvulsive therapy and novel brain stimulation modalities

2006 ◽  
Vol 8 (2) ◽  
pp. 241-258 ◽  
Keyword(s):  
Major Depression ◽  
Electroconvulsive Therapy ◽  
Brain Stimulation ◽  
Antidepressant Drugs ◽  
Treatment Modalities ◽  
Clinical Use ◽  
The Novel ◽  
Magnetic Seizure Therapy ◽  
Novel Treatments ◽  
Technological Methods

Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.

scholarly journals Study of correlation between perceived sleep disturbances in depressed patients with objective changes in sleep architecture using polysomnography before and after antidepressant therapy

2020 ◽  
Vol 8 (7) ◽  
pp. 2551
Author(s):  
Ganesh Ingole ◽  
Harpreet S. Dhillon ◽  
Bhupendra Yadav
Keyword(s):  
Sleep Disturbances ◽  
Total Sleep Time ◽  
Antidepressant Treatment ◽  
Sleep Onset ◽  
Sleep Time ◽  
Sleep Efficiency ◽  
Sleep Architecture ◽  
Wake Time ◽  
Depressed Patients ◽  
Before And After

Background: A prospective cohort study to correlate perceived sleep disturbances in depressed patients with objective changes in sleep architecture using polysomnography (PSG) before and after antidepressant therapy.Methods: Patients were recruited into the study after applying strict inclusion and exclusion criterion to rule out other comorbidities which could influence sleep. A diagnosis of Depressive episode was made based on ICD-10 DCR. Psychometry, in the form of Beck Depressive inventory (BDI) and HAMD (Hamilton depression rating scale) insomnia subscale was applied on Day 1 of admission. Patients were subjected to sleep study on Day 03 of admission with Polysomnography. Patients were started on antidepressant treatment post Polysomnography. An adequate trial of antidepressants for 08 weeks was administered and BDI score ≤09 was taken as remission. Polysomnography was repeated post remission. Statistical analysis was performed using Kruskal Wallis test and Pearson correlation coefficient.Results: The results showed positive (improvement) polysomnographic findings in terms of total sleep time, sleep efficiency, wake after sleep onset, percentage wake time and these findings were statistically significant. HAM-D Insomnia subscale was found to correlate with total sleep time, sleep efficiency, wake after sleep onset, total wake time and N2 Stage percentage.Conclusions: Antidepressant treatment effectively improves sleep architecture in Depressive disorder and HAM-D Insomnia subscale correlates with objective findings of total sleep time, sleep efficiency, wake after sleep onset, total wake time and duration of N2 stage of NREM.

Serotonergic Dysfunction in Depression

1989 ◽  
Vol 155 (S8) ◽  
pp. 25-31 ◽  
Author(s):  
Herbert Meltzer
Keyword(s):  
Tryptophan Hydroxylase ◽  
Rating Scale ◽  
Blood Platelets ◽  
Antidepressant Drugs ◽  
Depression Score ◽  
Plasma Tryptophan ◽  
Depressed Patients ◽  
Hydroxyindoleacetic Acid ◽  
Serotonergic Function ◽  
Neuroendocrine Challenge

Various irregularities in serotonin (5-HT) function have been postulated as causes of affective disorders. Serotonin has been related to many of the major symptoms of depression, e.g. mood, appetite, sleep, activity, and cognitive dysfunction. Interference with 5-HT synthesis or storage has been shown to induce depression in vulnerable individuals. Decreased levels of 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid, decreased plasma tryptophan, low tryptophan neutral amino acid ratio, abnormalities in serotonergic function indicated by neuroendocrine challenge tests and various platelet measures, have been reported in depressed patients. Concentrations of 5-HIAA, the major metabolite of 5-HT in plasma, were found to be significantly negatively correlated with severity of depression as measured by the Hamilton Rating Scale for Depression score and specific depressive symptoms, despite the fact that plasma 5-HIAA is largely peripheral in origin. Blood platelets, which have been suggested as models for serotonergic nerve terminals, have a significantly decreased number of 5-HT uptake sites and 3H-imipramine binding sites in depressed patients. Antidepressant drugs may act, in part, by enhancing serotonergic activity. The serotonergic deficit may occur at any of several levels: diminished availability of precursor, impaired activity of tryptophan hydroxylase, abnormalities in 5-HT release or uptake, 5-HT receptor abnormalities or interactions with other neurotransmitters.

The olfactory deficits of depressed patients are restored after remission with venlafaxine treatment

2020 ◽  
pp. 1-9
Author(s):  
Romain Colle ◽  
Khalil El Asmar ◽  
Céline Verstuyft ◽  
Pierre-Marie Lledo ◽  
Françoise Lazarini ◽  
...  
Keyword(s):  
Antidepressant Treatment ◽  
Depression Severity ◽  
Major Depressive ◽  
Depressed Patients ◽  
Before And After ◽  
Major Depressive Episodes ◽  
Depressive Episodes ◽  
Drug Free ◽  
A Current ◽  
Psychophysical Test

Abstract Background It is unclear whether olfactory deficits improve after remission in depressed patients. Therefore, we aimed to assess in drug-free patients the olfactory performance of patients with major depressive episodes (MDE) and its change after antidepressant treatment. Methods In the DEP-ARREST-CLIN study, 69 drug-free patients with a current MDE in the context of major depressive disorder (MDD) were assessed for their olfactory performances and depression severity, before and after 1 (M1) and 3 (M3) months of venlafaxine antidepressant treatment. They were compared to 32 age- and sex-matched healthy controls (HCs). Olfaction was assessed with a psychophysical test, the Sniffin’ Sticks test (Threshold: T score; Discrimination: D score; Identification: I score; total score: T + D + I = TDI score) and Pleasantness (pleasantness score: p score; neutral score: N score; unpleasantness score: U score). Results As compared to HCs, depressed patients had lower TDI olfactory scores [mean (s.d.) 30.0(4.5) v. 33.3(4.2), p < 0.001], T scores [5.6(2.6) v. 7.4(2.6), p < 0.01], p scores [7.5(3.0) v. 9.8(2.8), p < 0.001)] and higher N scores [3.5(2.6) v. 2.1(1.8), p < 0.01]. T, p and N scores at baseline were independent from depression and anhedonia severity. After venlafaxine treatment, significant increases of T scores [M1: 7.0(2.6) and M3: 6.8(3.1), p < 0.01] and p scores [M1: 8.1(3.0) and M3: 8.4(3.3), p < 0.05] were evidenced, in remitters only (T: p < 0.01; P: p < 0.01). Olfaction improvement was mediated by depression improvement. Conclusions The olfactory signature of MDE is restored after venlafaxine treatment. This olfaction improvement is mediated by depression improvement.

Effect of electroconvulsive therapy (ECT) on plasma tryptophan

1980 ◽  
Vol 10 (2) ◽  
pp. 377-380 ◽  
Author(s):  
L. J. Whalley ◽  
C. M. Yates ◽  
J. E. Christie
Keyword(s):  
Electroconvulsive Therapy ◽  
Acute Effect ◽  
Albumin Binding ◽  
Total Plasma ◽  
Plasma Tryptophan ◽  
Depressed Patients ◽  
Before And After ◽  
Free Plasma

SYNOPSISThe concentrations of total and free plasma tryptophan were measured in 12 unipolar depressed patients before and after a course of electroconvulsive therapy (ECT) and before and after single ECTs during the course of treatment. Eleven patients undergoing diagnostic cystoscopy served as controls to examine the acute effect of anaesthesia. Total and free plasma tryptophan concentrations in the depressed patients were not significantly different from control values and were not changed by the course of ECT. Free plasma tryptophan varied considerably within individual patients. Total plasma tryptophan was reduced acutely by ECT/anaesthesia in the depressed patients (P < 0·05) and by anaesthesia in the cystoscopy controls (P < 0·01). Free plasma tryptophan was not significantly altered. This reduction in total plasma tryptophan could be secondary to an effect of thiopentone on albumin binding of tryptophan.

Cognitive performance following fluoxetine treatment in depressed patients post myocardial infarction

2006 ◽  
Vol 18 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Jacqueline J. M. H. Strik ◽  
Adriaan Honig ◽  
Edwin Klinkenberg ◽  
Jeanette Dijkstra ◽  
Jelle Jolles
Keyword(s):  
Myocardial Infarction ◽  
Side Effects ◽  
Cognitive Performance ◽  
Antidepressant Treatment ◽  
Verbal Learning ◽  
Median Number ◽  
Double Blind ◽  
Depressed Patients ◽  
Before And After ◽  
Negative Side Effects

Background:As depression is a considerable risk factor for an unfavourable course of myocardial infarction (MI), antidepressant treatment of post-MI depression and, inherent to MI status, polypharmacy has become an important issue.Objective:The present study is the first to evaluate cognitive side effects of fluoxetine, as part of a placebo-controlled double-blind trial, in patients with post-first MI depression.Methods:Cognitive performance of 54 depressed patients post first-MI, treated with fluoxetine or placebo was compared. Cognitive performance was tested before and after 9 weeks of treatment using the Visual Verbal Learning Test, Concept Shifting Task, Stroop Colour-Word Test and Letter-Digit-Substitution Test.Results:The median number of cardiovascular drugs taken by MI patients was 4.9. There were no differences between the fluoxetine and the placebo group on cognitive performance.Conclusion:In sum, there were no negative side effects of fluoxetine compared with placebo on cognition in depressed MI patients, simultaneously treated with cardiac drugs.

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