Table 1.

Neurostimulation options for treatment of TRD.

Technique	Main stimulation target region	Mode of action	Evidence	Pro	Con
ECT	Cerebral cortex	Small currents and generalized seizure induction	Strong	First line therapy for patients who failed in pharmacotherapy, rapid antidepressive effects, long-lasting clinical experiences	Relapse rates, effort, cognitive side effects
tDCS	Cerebral cortex	Anode and cathode sending constant low current (0.5–2 mA) directly to the brain	Weak-moderate	Non-invasive, rapid effects	Less clinical experience
rTMS	Cerebral cortex	Magnetic pulses to depolarize cerebral neurons	Strong	Non-invasive, approved	Relapse rates, effort, small effect sizes
DBS	Nucleus accumbens, lateral habenula, ventral striatum, inferior thalamic nucleus, peduncle, subgenual cingulate	High-frequency stimulation (130–185 Hz); reduction of neuronal transmission by inactivating voltage-dependent ion channels; modulation of neuronal circuits	Moderate, experimental	Probably highly effective	Implantation procedure
MST	Cerebral cortex	Based on ECT, probably effects increased glucose metabolism	Weak-moderate	Less side effects than ECT	No broad evidence
CES	Probably affects limbic system, reticular activating system, hypothalamus	Electrical currents (<1 mA)	Weak-moderate	Non-invasive, supposed antidepressive mode of action, FDA-approved	No broad evidence
VNS	Left peripheral vagus nerve	(Long-term) modulation of neurotransmitters	Moderate-strong	Anti-suicidal effects and rates of remittance, combination option with nearly all other treatment options, FDA-approved	Latency in antidepressive efficacy