Disrupted metabolic support of intrinsic brain rhythms as a driver of spatiotemporal fragmentation in schizophrenia

Schizophrenia can involve disturbances of lived time, lived space, and pre-reflective selfhood. This Perspective examines whether impaired adaptation of cerebral energy metabolism to changing neural demand could provide a physiological constraint on the temporal and spatial organization of neural activity relevant to these experiences. Evidence from cellular models, magnetic resonance spectroscopy, metabolic imaging, electrophysiology, and functional neuroimaging is synthesized, with emphasis on oxidative capacity, respiratory reserve, high-energy phosphate transfer, glycolytic regulation, and metabolic-neural relationships. Across these levels, bioenergetic abnormalities are documented in schizophrenia, but the available evidence does not establish a uniform metabolic deficit or a causal chain from cellular metabolism to psychopathology. A testable hypothesis is therefore proposed: impaired metabolic adaptation may limit neural reconfiguration across functional states, including oscillatory synchronization, intrinsic neural timescale flexibility, and large-scale network differentiation. A staged multimodal assay is outlined, combining functional [18 F] FDG positron emission tomography and electroencephalography during graded 40-Hz auditory stimulation. Primary analyses test metabolic and neural demand-response functions and their relative scaling; secondary analyses address within-condition coupling, recruitment and recovery kinetics, and dimension-matched associations with lived time, lived space, and self-experience. The framework extends spatiotemporal psychopathology by specifying a candidate physiological mechanism while preserving the distinction between neural and experiential levels. It generates falsifiable predictions for mechanistic, longitudinal, and therapeutic studies in schizophrenia.