Abnormal brain oscillations, observed via electroencephalography

(EEG) and magnetoencephalography (MEG) are commonly reported in schizophrenia. Resting-state oscillatory findings have been inconsistent, likely because of the heterogeneity intrinsic to schizophrenia (such as age, symptoms, medications) as well as methodological issues (for example analysis procedures, EEG v.MEG). Most studies, however, observe more delta (1–4Hz) and theta (4–7Hz) resting-state activity in people with schizophrenia than in controls, with two recent meta-analyses concluding that enhanced low-frequency activity in schizophrenia is a robust finding. Although delta and theta oscillatory activity is common in stage 3 and 4 of slow-wave sleep, such activity during awake states is pathological, associated with traumatic brain injury, Alzheimer’s disease and brain lesions. Given increased slow-wave activity during the waking state in schizophrenia and given that individuals with schizophrenia typically do not show frank pathology on structural magnetic resonance imaging (MRI), it has been suggested that part of the brain in schizophrenia might be in an inactive ‘sleep-like state’ or that slow-wave activity in schizophrenia reflects subtle brain pathology. There appears to be some specificity for slow-wave abnormalities in schizophrenia. Slow-wave abnormalities are observed in unmedicated individuals with schizophrenia. Sponheim et al 11 found slow-wave abnormalities in both first episode schizophrenia as well as in individuals with chronic schizophrenia, suggesting that slow-wave abnormalities are stable characteristics of schizophrenia and not associated with treatment. Examining slowing in different psychiatric groups, Rockstroh et al reported that the spatial topography of slow-wave activity distinguishes individuals with schizophrenia from individuals with neurotic/affective diagnoses. Narayanan et al also reported that individuals with schizophrenia and their first-degree relatives showed augmented resting-state delta activity, whereas individuals with bipolar disorder and their first-degree relatives showed augmented fast alpha activity. Finally, Venables et al examined resting-state EEG activity in people with schizophrenia, bipolar disorder and their first-degree relatives. The authors found that abnormal low-frequency EEG resting activity was specific to people with schizophrenia and their relatives, as well as showing that abnormal slow-wave activity is associated with the Val158Met polymorphism of the COMT gene. Although abnormal slow-wave activity is frequently reported in EEG studies of schizophrenia, the reported source location or scalp distribution of slow-wave abnormalities in schizophrenia varies, with EEG studies reporting abnormal slowing in schizophrenia over posterior, frontal-midline and frontal-temporal regions. Inconsistency across EEG studies may be a result of variability in participants in the location of slow-wave pathology or because the scalp distribution of EEG power can be ambiguous. In particular, the conductivity of the skull creates a smearing effect such that the brain signals picked up by the electrodes are not necessarily from nearby generators. It may also be because both distributed and focal slow-wave activity contributes to EEG sensor activity and that, as a result, the location of the EEG reference electrode is an important factor in interpreting slow-wave scalp activity. MEG offers a reference-free method for assessing electromagnetic slow-wave activity that is not distorted by changes in conductivity across brain tissues. MEG has identified cortical generators of slow-wave activity in schizophrenia using singledipole source localisation. To our knowledge, only one MEG study has examined slow-wave activity at rest throughout the brain in schizophrenia. Using L2-minimum norm estimate localisation, Fehr et al 2 observed higher frontotemporal and posterior delta/theta activity in participants with