Several independent lines of evidence suggest the possible involvement of altered cerebral energy metabolism in the pathophysiology of schizophrenia. Imaging studies have used positron emission tomography (PET) with flurodeoxyglucose (FDG), or functional magnetic resonance imaging (fMRI), 15O magnetic resonance spectroscopy with 31P (31P-MRS) and single photon emission tomography (SPECT), to investigate cerebral metabolic rates in schizophrenia. Most but not all studies reveal decreased metabolism in the frontal cortex in schizophrenia, which was termed hypofrontality. Several studies also observed alterations in brain metabolic rates in other brain regions including the temporal lobes, the thalamus and the basal ganglia, leading to the suggestion of an impairment in the fronto-striatal-thalamic circuitry in schizophrenia rather than in a specific brain region (Andreasen et al. 1997). A direct link to phosphocreatine and ATP energy systems came from studies using 31P-MRS with or without chemical shift imaging, which enabled the measurement of ATP, phosphocreatine and inorganic phosphate. These studies showed reduced ATP in the frontal lobe and in left temporal lobe of schizophrenic patients as compared to controls (Volz et al. 2000). Altered brain energy metabolism could be due to impairment of mitochondria and a variety of studies reviewed recently by Ben Shachar (2002) suggest impaired mitochondrial energy metabolism in schizophrenia.