No evident neuronal damage after electroconvulsive therapy

被引:76
作者
Zachrisson, OCG [1 ]
Balldin, J
Ekman, R
Naesh, O
Rosengren, L
Ågren, H
Blennow, K
机构
[1] Univ Gothenburg, Inst Clin Neurosci, Dept Psychiat & Neurochem, Gothenburg, Sweden
[2] Karolinska Inst, Div Psychiat, Huddinge, Sweden
[3] Univ Gothenburg, Inst Clin Neurosci, Dept Neurol, Gothenburg, Sweden
[4] Lund Univ, Dept Anesthesia & Intens Care, Lund, Sweden
关键词
electroconvulsive therapy; depression; cerebrospinal fluid; tau; neurofilament; S-100; beta;
D O I
10.1016/S0165-1781(00)00202-X
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
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/giial damage or BBB dysfunction could be demonstrated following a therapeutic course of ECT. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:157 / 165
页数:9
相关论文
共 54 条
[1]  
ABRAMS R, 1992, ELECTROCONVULSIVE TH, P116
[2]   GLIAL FIBRILLARY ACIDIC PROTEIN IN THE CEREBROSPINAL-FLUID OF CHILDREN WITH AUTISM AND OTHER NEUROPSYCHIATRIC DISORDERS [J].
AHLSEN, G ;
ROSENGREN, L ;
BELFRAGE, M ;
PALM, A ;
HAGLID, K ;
HAMBERGER, A ;
GILLBERG, C .
BIOLOGICAL PSYCHIATRY, 1993, 33 (10) :734-743
[3]   A DOUBLE-BLIND EVALUATION OF ELECTROCONVULSIVE-THERAPY IN PARKINSONS-DISEASE WITH ON-OFF PHENOMENA [J].
ANDERSEN, K ;
BALLDIN, J ;
GOTTFRIES, CG ;
GRANERUS, AK ;
MODIGH, K ;
SVENNERHOLM, L ;
WALLIN, A .
ACTA NEUROLOGICA SCANDINAVICA, 1987, 76 (03) :191-199
[5]  
[Anonymous], PRACT EL THER REC TR
[6]   DETERMINATION OF S-100 AND GLIAL FIBRILLARY ACIDIC PROTEIN CONCENTRATIONS IN CEREBROSPINAL-FLUID AFTER BRAIN INFARCTION [J].
AURELL, A ;
ROSENGREN, LE ;
KARLSSON, B ;
OLSSON, JE ;
ZBORNIKOVA, V ;
HAGLID, KG .
STROKE, 1991, 22 (10) :1254-1258
[7]   Serum neuron-specific enolase levels do not increase after electroconvulsive therapy [J].
Berrouschot, J ;
Rolle, K ;
Kuhn, HJ ;
Schneider, D .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1997, 150 (02) :173-176
[8]  
Blennow K, 1998, J NEURAL TRANSM-SUPP, P223
[9]   tau protein in cerebrospinal fluid - A biochemical marker for axonal degeneration in Alzheimer disease? [J].
Blennow, K ;
Wallin, A ;
Agren, H ;
Spenger, C ;
Siegfried, J ;
Vanmechelen, E .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1995, 26 (03) :231-245
[10]  
Boiteux J, 1997, ENCEPHALE, V23, P21