ERPLAB toolbox is a freely available, open-source toolbox for processing and analyzing event-related potential (ERP) data in the MATLAB environment. ERPLAB is closely integrated with EEGLAB, a popular open-source toolbox that provides many EEG preprocessing steps and an excellent user interface design. ERPLAB adds to EEGLAB’s EEG processing functions, providing additional tools for filtering, artifact detection, re-referencing, and sorting of events, among others. ERPLAB also provides robust tools for averaging EEG segments together to create averaged ERPs, for creating difference waves and other recombinations of ERP waveforms through algebraic expressions, for filtering and re-referencing the averaged ERPs, for plotting ERP waveforms and scalp maps, and for quantifying several types of amplitudes and latencies. ERPLAB’s tools can be accessed either from an easy-to-learn graphical user interface or from MATLAB scripts, and a command history function makes it easy for users with no programming experience to write scripts. Consequently, ERPLAB provides both ease of use and virtually unlimited power and flexibility, making it appropriate for the analysis of both simple and complex ERP experiments. Several forms of documentation are available, including a detailed user’s guide, a step-by-step tutorial, a scripting guide, and a set of video-based demonstrations.

Mismatch negativity (MMN) deficits in schizophrenia (SCZ) have been studied extensively since the early 1990s, with the vast majority of studies using simple auditory oddball task deviants that vary in a single acoustic dimension such as pitch or duration. There has been a growing interest in using more complex deviants that violate more abstract rules to probe higher order cognitive deficits. It is still unclear how sensory processing deficits compare to and contribute to higher order cognitive dysfunction, which can be investigated with later attention-dependent auditory event-related potential (ERP) components such as a subcomponent of P300, P3b. In this meta-analysis, we compared MMN deficits in SCZ using simple deviants to more complex deviants. We also pooled studies that measured MMN and P3b in the same study sample and examined the relationship between MMN and P3b deficits within study samples. Our analysis reveals that, to date, studies using simple deviants demonstrate larger deficits than those using complex deviants, with effect sizes in the range of moderate to large. The difference in effect sizes between deviant types was reduced significantly when accounting for magnitude of MMN measured in healthy controls. P3b deficits, while large, were only modestly greater than MMN deficits (d=0.21). Taken together, our findings suggest that MMN to simple deviants may still be optimal as a biomarker for SCZ and that sensory processing dysfunction contributes significantly to MMN deficit and disease pathophysiology.

Objective: The ability to perceive the motion of biological objects, such as faces, is a critical component of daily function and correlates with the ability to successfully navigate social situations (“social cognition”). Deficits in motion perception in schizophrenia were first demonstrated ~20 years ago but remain understudied, especially within the early, potentially prodromal, stages of the illness. The authors examined the neural bases of visual sensory-processing impairments, including motion, in schizophrenia and attenuated psychosis (clinical high risk) patients relative to age-matched controls. Methods: Electrophysiological recordings during stimulus and motion processing were analyzed using oscillatory (“time frequency”) approaches that differentiated motion-onset evoked activity from stimulusonset sensory-evoked responses. These were compared to functional MRI measures of motion processing. Results: Significant deficits in motion processing were observed across the schizophrenia and attenuated psychosis populations and these deficits predicted impairments in both face-emotion recognition and cognitive function. In contrast to motion, sensory-evoked stimulus-onset responses were intact in attenuated psychosis individuals and, further, the relative deficit in motion-versus stimulus-onset responses predicted transition to schizophrenia. In schizophrenia patients, motion detection deficits mapped to impaired activation of motion-sensitive visual cortex (area MT+) during fMRI. Additional visual impairments in schizophrenia patients, not present in individuals with attenuated psychosis, implicated other visual regions, including the middle occipital gyrus and the pulvinar thalamic nucleus. Conclusions: The present study emphasizes the importance of sensory-level visual dysfunction in the etiology and personal experience of individuals with schizophrenia, and demonstrates that motion processing deficits may predate illness onset and contribute to impaired function even in clinical high risk, attenuated psychosis patients.