No abstract

A review of the literature was performed, including technical and pharmacologic methods tested to date to alleviate the cognitive side effects of ECT. Technical changes included electrode placement and stimulus waveform. Pharmacological methods included NMDA-receptor antagonists, cyclooxygenase inhibitors, calcium channel blockers, cholinesterase inhibitors, glucocorticoid receptor antagonists, thyroid hormones, opioid antagonists, nitric oxide donors, and nootropic agents. Results: Approaches to reduce ECT-related cognitive side effects have been inconsistent. Neuroinflammation, involved in the pathophysiology of numerous neuropsychiatric conditions, may also contribute via immune mechanisms. Microglia in a neurotoxic state produce pro-inflammatory mediators (IL-1b, TNF-a, IL-6), whereas the neuroprotective phenotype release anti-inflammatory cytokines (IL-10). The microbiome may also play a role via immune signaling mechanisms. Interestingly, a case report has shown changes in gut microbiome bacterial populations during a course of ECT. Conclusions: Given that ECT induces seizures, the finding that the adverse effects of epileptic seizures may be caused by neuroinflammation mediated by pro-inflammatory glial cells may be applicable to the treatment of MDD. This connection suggests the possibility of the microbiome affecting inflammatory pathways related to the cognitive side effects of ECT. Nonetheless, further work is needed to evaluate the neurobiological underpinnings of ECT-induced cognitive side effects as facilitated by neuroinflammatory pathways and changes in the microbiome.