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Magnetic resonance (MR) spectroscopic measurement of γ-aminobutyric acid (GABA) in major depression before and after electroconvulsive therapy

Published online by Cambridge University Press:  06 August 2018

Marie Krøll Knudsen*
Affiliation:
Center of Functionally Integrative Neuroscience, Aarhus University Hospital, Aarhus, Denmark
Jamie Near
Affiliation:
Department of Psychiatry, Douglas Mental Health University Institute, McGill University, Montreal, Canada Department of Biomedical Engineering, McGill University, Montreal, Canada
Anne Bastholm Blicher
Affiliation:
Department of Psychiatry, Aarhus University Hospital Risskov, Aarhus, Denmark
Poul Videbech
Affiliation:
Mental Health Centre Glostrup, Copenhagen University Hospital, Glostrup, Denmark
Jakob Udby Blicher
Affiliation:
Center of Functionally Integrative Neuroscience, Aarhus University Hospital, Aarhus, Denmark
*
*Author for correspondence: Dr. Marie Krøll Knudsen, Center of Functionally Integrative Neuroscience, Aarhus University Hospital, Nørrebrogade 44, building 10G, 5th floor, 8000 Aarhus C, Denmark. Tel: +45 4114 2216; Fax: +45 7846 4400; E-mail: [email protected]

Abstract

Objective

Prior studies suggest that a dysregulation of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) is involved in the pathophysiology of major depression. We aimed to elucidate changes in cortical GABA content in relation to depression and electroconvulsive therapy (ECT) using magnetic resonance spectroscopy (MRS).

Methods

In total, 11 patients with major depression or depressive episode of bipolar disorder (mean pre-ECT Ham-17 of 26) and 11 healthy subjects were recruited. GABA was quantified using short-TE MRS in prefrontal and occipital cortex. Other neurometabolites such as glutathione (GSH), N-acetylaspartate (NAA) and glutamate (Glu) were secondary outcome measures.

Results

No significant differences in GABA/Cr levels were observed between patients at baseline and healthy subjects in prefrontal cortex, t(20)=0.089, p=0.93 or occipital cortex t(21)=0.37, p=0.72. All patients improved on Ham-17 (mean post-ECT Ham-17 of 9). No significant difference was found in GABA, Glu, glutamine, choline or GSH between pre- and post-ECT values. However, we observed a significant decrease in NAA levels following ECT t(22)=3.89, p=0.0038, and a significant correlation between the NAA decline and the number of ECT sessions p=0.035.

Conclusions

Our study does not support prior studies arguing for GABA as a key factor in the treatment effect of ECT on major depression. The reduction in NAA levels following ECT could be due to neuronal loss or a transient dysfunction in prefrontal cortex. As no long-term follow-up scan was performed, it is unknown whether NAA levels will normalise over time.

Type
Original Article
Copyright
© Scandinavian College of Neuropsychopharmacology 2018 

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