Neurophysiological distinction between schizophrenia and schizoaffective disorder

• Main Authors: Daniel H Mathalon, Ralph E Hoffman, Todd D Watson, Ryan M Miller, Brian J Roach, Judith M Ford
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2010-01-01
• Series: Frontiers in Human Neuroscience
• Subjects: Schizophrenia; EEG; P300; event-related potential; schizoaffective disorder
• Online Access: http://journal.frontiersin.org/Journal/10.3389/neuro.09.070.2009/full

Schizoaffective disorder (SA) is distinguished from schizophrenia (SZ) based on the presence of prominent mood symptoms over the illness course. Despite this clinical distinction, SA and SZ patients are often combined in research studies, in part because data supporting a distinct pathophysiological boundary between the disorders are lacking. Indeed, few studies have addressed whether neurobiological abnormalities associated with SZ, such as the widely replicated reduction and delay of the P300 event-related potential (ERP), are also present in SA. Scalp EEG was acquired from patients with DSM-IV SA (n=15) or SZ (n=22), as well as healthy controls (HC; n=22) to assess the P300 elicited by infrequent target (15%) and task-irrelevant distractor (15%) stimuli in separate auditory and visual “oddball” tasks. P300 amplitude was reduced and delayed in SZ, relative to HC, consistent with prior studies. These SZ abnormalities did not interact with stimulus type (target vs. task-irrelevant distractor) or modality (auditory vs. visual). Across sensory modality and stimulus type, SA patients exhibited normal P300 amplitudes (significantly larger than SZ patients and indistinguishable from HC). However, P300 latency and reaction time were both equivalently delayed in SZ and SA patients, relative to HC. P300 differences between SA and SZ patients could not be accounted for by variation in symptom severity, socio-economic status, education, or illness duration. Although both groups show similar deficits in processing speed, SA patients do not exhibit the P300 amplitude deficits evident in SZ, consistent with an underlying pathophysiological boundary between these disorders.