Unaltered neuronal and glial counts in animal models of magnetic seizure therapy and electroconvulsive therapy.

Published

Journal Article

Anatomical evidence of brain damage from electroconvulsive therapy (ECT) is lacking; but there are no modern stereological studies in primates documenting its safety. Magnetic seizure therapy (MST) is under development as a less invasive form of convulsive therapy, and there is only one prior report on its anatomical effects. We discerned no histological lesions in the brains of higher mammals subjected to electroconvulsive shock (ECS) or MST, under conditions that model closely those used in humans. We sought to extend these findings by determining whether these interventions affected the number of neurons or glia in the frontal cortex or hippocampus. Twenty-four animals received 6 weeks of ECS, MST, or anesthesia alone, 4 days per week. After perfusion fixation, numbers of neurons and glia in frontal cortex and hippocampus were determined by unbiased stereological methods. We found no effect of either intervention on volumes or total number or numerical density of neurons or glia in hippocampus, frontal cortex, or subregions of these structures. Induction of seizures in a rigorous model of human ECT and MST therapy does not cause a change in the number of neurons or glia in potentially vulnerable regions of brain. This study, while limited to young, healthy, adult subjects, provides further evidence that ECT and MST, when appropriately applied, do not cause structural damage to the brain.

Full Text

Duke Authors

Cited Authors

  • Dwork, AJ; Christensen, JR; Larsen, KB; Scalia, J; Underwood, MD; Arango, V; Pakkenberg, B; Lisanby, SH

Published Date

  • December 2009

Published In

Volume / Issue

  • 164 / 4

Start / End Page

  • 1557 - 1564

PubMed ID

  • 19782728

Pubmed Central ID

  • 19782728

Electronic International Standard Serial Number (EISSN)

  • 1873-7544

International Standard Serial Number (ISSN)

  • 0306-4522

Digital Object Identifier (DOI)

  • 10.1016/j.neuroscience.2009.09.051

Language

  • eng