Furthermore, recovery after stroke will, in most cases, imply compensatory shifts in cross-regional interactions (Gerloff et al., 2006, van Meer et al., 2010 and Carter et al., 2012). Envelope ICMs involving somatomotor, executive, and attention networks

are well investigated in stroke and during recovery and have been shown to be predictive for both behavioral deficits and adaptive reorganization after stroke (Carter et al., 2010 and Wang et al., 2010). This holds, in particular, for interhemispheric coupling in these networks (Carter et al., 2012). In contrast, evidence regarding changes in phase ICMs is limited to a few recent studies. Alpha-band ICMs have been observed to be decreased in perilesional and increased SCR7 supplier in contralesional regions, and this interhemispheric difference has been found to predict cognitive and motor performance as well as aspects of poststroke recovery (Westlake et al., 2012 and Dubovik et al., 2012). Moreover, ongoing beta-band interhemispheric coupling was found to change under the influence of rehabilitation training (Pellegrino et al., 2012). In PD, numerous studies have addressed changes in ICMs. Substantial Neratinib concentration evidence has accumulated demonstrating that phase ICMs are altered in specific ways in PD and that they correlate with

clinical symptoms and behavior. Many of the studies in PD patients involve recordings from basal ganglia structures during stereotactic surgery for deep brain stimulation. These provide clear evidence for abnormal beta-band ICMs in corticobasal ganglia loops (Figure 5A), which correlate with severity of bradykinesia and rigidity, the key clinical symptoms in PD (Brown, 2003 and Stein and Bar-Gad, 2013). Accordingly, their suppression by dopaminergic medication or deep brain stimulation ameliorates

the patient’s condition. These findings have also been confirmed by MEG studies of phase ICMs in PD (Stoffers et al., 2008 and Litvak et al., 2011). Interestingly, dopaminergic therapy and reduction of motor impairment are associated with the emergence of a gamma-band ICM between cortex and basal ganglia (Brown, 2003 and Jenkinson et al., 2013) (Figure 5B). Overall, these studies have led to the notion of movement-permissive (gamma-band) versus movement-prohibitive (beta-band) ICMs (Brown, 2003) (Figure 5C). More generally, it has been suggested that these ICMs permit or prohibit enough a change in the sensorimotor or cognitive set (Engel and Fries, 2010). Studies on envelope ICMs using fMRI have observed increased coupling between cortex and basal ganglia in PD that is attenuated by dopamine (Kwak et al., 2010 and Baudrexel et al., 2011). Whether this might relate to power envelope correlations of the abundant beta-band activity has apparently not yet been tested. In schizophrenia, functional disconnection in brain networks has been considered an important pathophysiological mechanism already early on (Friston and Frith, 1995).