Although the antidepressant mechanism of ECT is unknown, there are data to support noradrenergic involvement. Patients who had been recently successfully treated with ECT for major depression were studied in a randomized double-blind cross-over design comparing catecholamine depletion using alpha-methyl-para-tyrosine to a placebo procedure. Mean MADRS scores at baseline (4.2 SD 2.7) and following depletion (4.6 SD 1.1) were similar, despite a 57.7% decrease in serum homovanillic acid (HVA) and a 61.5% decrease in 3-methoxy-4-hydroxyenylethyleneglycol (MHPG). These data suggest that catecholamine availability may not be necessary for acutely maintaining an antidepressant response to ECT.
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http://dx.doi.org/10.1016/j.pnpbp.2009.04.005 | DOI Listing |
Eur J Drug Metab Pharmacokinet
January 2025
Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Ultimo, NSW, 2007, Australia.
Caffeine consumption is regarded as a widespread phenomenon, and its usage has continued to increase. In addition, the growing usage of antidepressants worldwide and increase in mental health disorders were shown in recent statistical analyses conducted by the World Health Organisation. The coadministration of caffeine and antidepressants remains a concern due to potential interactions that can alter a patient's response to therapy.
View Article and Find Full Text PDFAlterations in the kynurenine pathway, and in particular the balance of neuroprotective and neurotoxic metabolites, have been implicated in the pathophysiology of Major Depressive Disorder (MDD) and antidepressant treatment response. In this study, we examined the relationship between changes in kynurenine pathway activity (Kynurenine/Tryptophan ratio), focusing on the balance of neuroprotective-to neurotoxic metabolites (Kynurenic Acid/Quinolinic Acid and Kynurenic Acid/3-Hydroxykynurenine ratios), and response to 8 weeks of selective serotonin reuptake inhibitor (SSRI) treatment, including early changes four weeks after SSRI initiation. Additionally, we examined relationships between kynurenine metabolite ratios and three promising biomarkers of depression and antidepressant response: amygdala/hippocampal volume, and glutamate metabolites in the anterior cingulate cortex.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.
Purpose: This study aimed to assess the protective effect of a clinical dose esketamine on cerebral ischemia/reperfusion (I/R) injury and to reveal the potential mechanisms associated with microglial polarization and autophagy.
Methods: Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in adult rats and simulated by oxygen-glucose deprivation (OGD) in BV-2 microglial cells. Neurological and sensorimotor function, cerebral infarct volume, histopathological changes, mitochondrial morphological changes, and apoptosis of ischemic brain tissues were assessed in the presence or absence of esketamine and the autophagy inducer rapamycin.
Cureus
December 2024
Psychiatry, Dr. Kamal Psychiatric Hospital, Bethlehem, PSE.
Dissociation is a cognitive process that disrupts consciousness, identity, or memory. It is frequently used as a form of defense in response to significant stress or trauma. In serious situations, it might show as a dissociative disorder, which extremely impairs psychological functioning.
View Article and Find Full Text PDFAME Case Rep
November 2024
Faculty of Medicine, Imperial College London, London, UK.
Background: Serotonin syndrome is an adverse drug reaction characterised by the excess of serotonin activity in the central nervous system. It is a condition of great concern in primary care where some patients, usually with treatment-resistant depression, get treatment with multiple serotonergic agents.
Case Description: This retrospective case series looked at 20 primary care patients with treatment-resistant depression who developed mild serotonin syndrome after starting a second antidepressant.
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