EEG-based neurofeedback (EEG-NF) has the advantage of being more widely available and including ambulatory settings. It is a popular procedure, especially in child and adolescent mental health

settings in application to attention deficit/ hyperactivity- disorder (ADHD),5,6 although a recent meta-analysis has raised doubts about the specificity- of the effects in ADHD.7 Several studies that have also been conducted with EEG-NF in depression will be reviewed below. Compared with deep brain stimulation (DBS),8,9 fMRI-NF has the advantage of noninvasiveness and spatial flexibility. Inhibitors,research,lifescience,medical However, it is too early to make any direct comparisons of the clinical effects of these two techniques in psychiatry,

which have so far been used for very different Inhibitors,research,lifescience,medical patient populations due to the restriction of DBS to severe and treatment-refractory cases. Neurofeedback also differs from all external stimulation techniques in that it enables the patients themselves to control their brain activity and thus to contribute to their experience of self-efficacy, which may be an important therapeutic factor.10 This aspect will be discussed in more detail below, Inhibitors,research,lifescience,medical in the section of links between neurofeedback and social learning theory. There are, in principle, at least two ways in which selfregulation of brain activity through neurofeedback may be beneficial for depression and other mental disorders. Self -regulation training might address a primary abnormal process, such as hyper- or hypoactivation

of specific brain areas Inhibitors,research,lifescience,medical or networks. For this approach, it would be necessary to identify such abnormal activation patterns in individual patients beforehand. Although research with the fMRI technique (and metabolic imaging with positron emission Inhibitors,research,lifescience,medical tomography, PET) has yielded several potential disease-relevant targets for depression, notably imbalances between CP-690550 ic50 prefrontal and limbic areas,11-12 none of these have been validated as biomarkers for use in individual patients. Similarly, although intriguing results have been obtained with EEG mapping techniques in relation to hemispheric asymmetries in depression (see EEG Thiamine-diphosphate kinase section below), these have not attained individual biomarker status either. At the present time, there is insufficient evidence to identify any reliably abnormal, local, or distributed brain activation patterns in individual patients with depression that could be targeted with neurofeedback (or indeed, any other neuromodulation technique, including DBS). However, neuromodulation can also act in a different way, by activating or suppressing circuits that are not primarily abnormal, but whose modulation may nevertheless produce clinical benefits.