title: No evident neuronal damage after electroconvulsive therapy.
abstract: Electroconvulsive therapy (ECT) is regarded as one of the most effective treatments for major depressive disorder but has also been associated with cognitive deficits possibly reflecting brain damage. The aim of this study was therefore to evaluate whether ECT induces cerebral damage as reflected by different biochemical measures. The concentrations in the cerebrospinal fluid (CSF) of three established markers of neuronal/glial degeneration, tau protein (tau), neurofilament (NFL) and S-100 beta protein, were determined in nine patients who fulfilled DSM-IV criteria for major depression. CSF samples were collected before and after a course of six ECT sessions. The CSF/serum (S) albumin ratio reflecting potential blood-brain barrier (BBB) dysfunction was also determined at these time points. The treatment was clinically successful with a significant decline of depressive symptoms in all patients as assessed by the Montgomery-Asberg Rating Scale for Depression. Several patients had signs of BBB dysfunction and/or neuronal damage before the start of treatment. Levels of CSF-tau, CSF-NFL and CSF-S-100 beta levels were not significantly changed by ECT. Also the CSF/S albumin ratio was found to be unchanged after the course of ECT. In conclusion, no biochemical evidence of neuronal/glial damage or BBB dysfunction could be demonstrated following a therapeutic course of ECT.
authors.affiliation: Institute of Clinical Neuroscience, Department of Psychiatry and Neurochemistry, Göteborg University, Göteborg, Sweden. olof.zachrisson@neuro.gu.se
authors.forename: O C
authors.initials: OC
authors.lastname: Zachrisson
authors.forename: J
authors.initials: J
authors.lastname: Balldin
authors.forename: R
authors.initials: R
authors.lastname: Ekman
authors.forename: O
authors.initials: O
authors.lastname: Naesh
authors.forename: L
authors.initials: L
authors.lastname: Rosengren
authors.forename: H
authors.initials: H
authors.lastname: Agren
authors.forename: K
authors.initials: K
authors.lastname: Blennow
mesh_terms: D000328:Adult; D000368:Aged; D001714:Bipolar Disorder / Q000134:cerebrospinal fluid / Q000628:therapy*; D001812:Blood-Brain Barrier / Q000502:physiology; D001925:Brain Damage, Chronic / Q000134:cerebrospinal fluid / Q000175:diagnosis / Q000209:etiology*; D003865:Major Depressive Disorder / Q000134:cerebrospinal fluid / Q000628:therapy*; D004565:Electroconvulsive Therapy; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009414:Nerve Growth Factors; D016900:Neurofilament Proteins / Q000134:cerebrospinal fluid; D012307:Risk Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000134:cerebrospinal fluid; D016896:Treatment Outcome; D016875:tau Proteins / Q000134:cerebrospinal fluid
chemical_list: D009414:Nerve Growth Factors; D016900:Neurofilament Proteins; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D016875:tau Proteins