The evidence reviewed strongly suggests that CP may be understood as the result of a localized reverberation loop between the parietal cortex (SI, and perhaps SII) and the sensory thalamus (Vc, core and shell) with a supporting role of Vim, CL and its SI projections, and pulvinar (Canavero et al. 1993; Canavero 1994), as this is the only mechanism able to explain pain disappearance following lesions limited to the subcortical white matter (see Box 8.1). This dipole is exquisitely adjusted to explain somatotopographical pain distribution in CP (Canavero 1994). The loop, with its descending excitatory arm, is engaged bilaterally, with contralateral – or, in some cases, ipsilateral – predominance. In those rare cases with complete SI or thalamic destruction (e.g., maxithalamotomies), the reverberant loop can be activated contralaterally. CP appears to be more frequent after right-sided lesions, perhaps due to lateralization of norepinephrine. Since the evidence points to a major role of this arm in CP sustenance (see also Yamashiro et al. 1991), we propose that STT lesions (or simple interference, without actual sensory loss) unbalance the normal oscillatory corticothalamic “dialogue,” starting in SI, where GABA levels drop acutely, and induce changes caudad along a diffuse spinotruncothalamic reticular core (see in Gybels and Sweet 1989; Nandi et al. 2004), which becomes hyperactive.