Objective: The purpose of this study was to evaluate whether ECT cause
s structural brain damage. Method: The literature review covered the f
ollowing areas: cognitive side effects, structural brain imaging, auto
psies of patients who had received ECT, post-mortem studies of epilept
ic subjects, animal studies of electroconvulsive shock (ECS) and epile
psy, and the neuropathological effects of the passage of electricity,
heat generation, and blood-brain barrier disruption. Results: ECT-indu
ced cognitive deficits are transient, although spotty memory loss may
persist for events immediately surrounding the ECT course. Prospective
computerized tomography and magnetic resonance imaging studies show n
o evidence of ECT-induced structural changes. Some early human autopsy
case reports from the unmodified ECT era reported cerebrovascular les
ions that were due to agonal changes or undiagnosed disease. la animal
ECS studies that used a stimulus intensity and frequency comparable t
o human ECT, no neuronal loss was seen when appropriate control animal
s, blind ratings, and perfusion fixation techniques were employed. Con
trolled studies using quantitative cell counts have failed to show neu
ronal loss even after prolonged courses of ECS. several well-controlle
d studies have demonstrated that neuronal loss occurs only after 1.5 t
o 2 hours of continuous seizure activity in primates, and adequate mus
cle paralysis and oxygenation further delay these changes. These condi
tions are not approached during ECT. Other findings indicate that the
passage of electricity, thermal effects, and the transient disruption
of the blood-brain barrier during ECS do not result in structural brai
n damage. Conclusions: There is no credible evidence that ECT causes s
tructural brain damage.