The functional deficit after a focal brain lesion is determined by the localization and the extent of the tissue damage. Since destroyed tissue usually cannot be replaced in the adult human brain, improvement or recovery of neurological deficits can be achieved only by reactivation of functionally disturbed but morphologically preserved areas or by recruitment of alternative pathways within the functional network. The visualization of disturbed interaction in functional networks and of their reorganization in the recovery after focal brain damage is the domain of functional imaging modalities such as positron emission tomography (PET). Longitudinal assessments at rest and during activation tasks during the early and later periods following a stroke can demonstrate recruitment and compensatory mechanisms in the functional network responsible for complete or partial recovery of disturbed functions. Imaging studies have shown that improvements after focal cortical injury are represented over larger cortical territories. It has also been shown that the unaffected hemisphere in some instances actually inhibits the recovery of ipsilateral functional networks and this effect of transcallosal inhibition can be reduced by non-invasive brain stimutation. Non-invasive brain stimulation (NIBS) can modulate the excitability and activity of targeted cortical regions and thereby alter the interaction within pathologically affected functional networks; this kind of intervention might promote the adaptive cortical reorganization of functional networks after stroke. In poststroke aphasia several studies attempted to restore perilesional neuronal activity in the injured left inferior frontal gyrus by applying excitatory high frequency repetitive transcranial magnetic stimulation (rTMS) or intermittent theta burst stimulation (iTBS) or anodal transcranial direct current stimulation (tDCS), but most NIBS studies in poststroke aphasia employed inhibitory low frequency rTMS for stimulation of the contralesional pars triangularis of the right inferior frontal gyrus (BA 45) in order to reduce right hemisphere hyperactivity and transcallosal inhibition on the left Broca's area. While most studies reported single cases or small case series with chronic poststroke aphasia without any control condition, only a few controlled studies including sham stimulation were performed in chronic stage after stroke. In one controlled randomized study changes in PET activation pattern in the subacute course were related to the clinical improvement. In this "proof-of-principle" study the shift of the activation pattern to the dominant hemisphere induced by inhibitory rTMS over the right inferior frontal gyrus could be demonstrated in the PET activation studies and correlated to improved performance in aphasia tests. NIBS might be a treatment strategy which could improve the effect of other rehabilitative efforts.