Abstract

Though there are many caveats when trying to relate modulatory effects of repetitive transcranial magnetic stimulation (rTMS) in the rodent brain to rTMS effects in humans, the preclinical findings provide an explanation for the possible neurobiological mechanisms underlying the therapeutic effects reported in numerous clinical trials. There is accumulating evidence that acute rTMS of frontal brain regions leads to alterations in mesolimbic and mesostriatal release patterns of dopamine in vivo . Dopamine-active antidepressant treatment strategies may be of particular benefit in a subgroup of patients with a low level of dopamine function, as reflected by symptoms such as anhedonia, marked psychomotor retardation or concomitant Parkinson's disease. Therefore, with respect to the design of clinical trials, the identification of such patients with a putative deficit in dopaminergic neurotransmission related to psychopathology might lead to a better antidepressant efficacy of rTMS beyond the only moderate and rather short-lived therapeutic effects reported so far. In support of this hypothesis are findings that depressed patients suffering from psychotic symptoms poorly respond to rTMS.

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