Meta-analyses and mega-analyses of structural magnetic resonance imaging (sMRI) and diffusion MRI (dMRI) studies in thousands of people with schizophrenia have shown reduced brain volumes and structural connectivity relative to healthy controls, some of which consistently correlate with the severity of symptoms and cognitive impairment. Post-mortem studies point to a pathophysiology of reduced neuronal size and dendritic arborisation, which is multifactorial. Magnetic resonance spectroscopy (MRS) reductions in N-acetyl-aspartate in some regions and reduced glucose uptake in the pre-frontal cortex (PFC) on positron emission tomography (PET) both suggest impaired cerebral mitochondrial metabolism. MRS studies also suggest glutamatergic abnormalities, which other studies suggest may be the primary neurochemistry of schizophrenia, while fluorodopa PET shows increased dopamine turnover in the striatum as the likely cause of psychotic symptoms. Single-photon emission computed tomography (SPECT) and PET measured blood flow are both reduced in the PFC, compounded by age, chronicity and antipsychotic medication. The functional imaging literature, including functional magnetic resonance imaging (fMRI), consistently points to the superior temporal gyrus (STG) and connected regions as the areas underpinning auditory hallucinations. Resting state fMRI is delivering consistent findings of dysconnectivity in schizophrenia, and studies of learning and reward are linking physiology, pharmacology and phenomenology. Necessarily, this is a very technical review. Box 7.1 presents a lay summary of the chapter. Overall, the vast neuroimaging literature in schizophrenia can be summarised as showing premorbid structural and functional changes that probably become more pronounced, especially in prefrontal and temporal lobes (reflecting reduced top-down cognitive control and input from the regularities of experience respectively), as people develop psychosis, driven by increased dopamine synthesis and turnover, with some likely progression in general and in those with a poor outcome. None of these findings has, however, been shown to be specific to schizophrenia, and there are generally similar but lesser changes in bipolar disorder. Progress in scientific understanding and evaluating clinical applications will require clear hypotheses, adequately powered studies, standardised methods and reporting.