Purpose: Attribution of different symptoms in schizophrenia patients according to distinctive patterns of brain dysfunction. Methods: A review of the research work on three nodal hubs. These hubs are: 1) Thalamocortical and thalamosubcortical connections, 2) Glutamate deficit at the granule cells in dentate gyrus leading to enhanced hippocampal pyramidal neurons activity, and 3) Dysconnections at the Salience Network (SN), between Anterior Insula, (IA) associated with Default Mode Network (DMN) and dorsal anterior cingulate cortex (dACC), associated with Central executive network (CEN). Results: Imbalance of thalamocortical projections including hypoconnectivity between mediodorsal thalamus and dorsolateral and dorsomedial prefrontal cortices and anterior thalamic nuclei with anterior cingulate gyri causing cognitive deficits together with hyperconnectivity between ventrolateral thalamic nuclei and sensorimotor, auditive and visual regions and subcortical extensions causing psychotic symptoms. Psychotic contents emerged from the dentate-hippocampal region through enhanced pyramidal neurons activity following disinhibition secondary to glutamate receptors deficits at the dentate gyrus granule cell. Disconnection of anterior insula with dorsal anteriorcingular cortices (salience network, SN) and some regions of the central executive (CEN) and default mode network (DMN) can provoke aberrancies and coactivation of networks with difficulties to distinguish outside world from oneself. Conclusion: There are three nodal hubs in the physiopathology of schizophrenia. Imbalance of thalamocortical connections in line with cognitive disturbances, enhanced hippocampal activity linked with generation of psychotic contents and disconnectivity of anterior insula leading to confusion between external world and oneself and in some cases unawareness of personal identity.