COGNITIVE NEUROSCIENCE AND NEUROPSYCHOLOGY NEUROREPORT 0959-4965 & Lippincott Williams & Wilkins Vol 12 No 17 4 December 2001 3815 Early visual processing deficits in schizophrenia: impaired P1 generation revealed by high-density electrical mapping John J. Foxe, 1,2,3,CA Glen M. Doniger 1,4 and Daniel C. Javitt 1,5 1 Cognitive Neurophysiology Laboratory, Cognitive Neuroscience and Schizophrenia Program, Nathan S. Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962; 2 Department of Neuroscience and 3 Department of Psychiatry and Behavioural Science, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461; 4 Department of Psychology, New York University, New York, NY; 5 Department of Psychiatry, New York University School of Medicine, 550 1st Avenue, New York, NY 10016, USA CA,1 Corresponding Author and Address Received 22 August 2001; accepted 26 September 2001 Integrity of early visual sensory processing in schizophrenia was assessed using the well characterized P1 and N1 components of the visual evoked potential (VEP) as our dependent meas- ures. VEPs were recorded in response to successively less fragmented line drawings of common objects. P1 amplitudes were significantly reduced across all stimulus conditions for patients versus controls. Further, this decrement was relatively greater at parieto-occipital than occipito-temporal electrode sites. No differences in N1 amplitude were found. The finding of P1 deficits in patients, particularly over dorsal scalp, supports the view that schizophrenia is associated with impairment of early dorsal visual stream processing. On the other hand, the finding of normal N1 amplitudes in patients suggests that early stages of ventral stream processing may be relatively more intact. These results imply that the cognitive impairment seen in schizophrenia is not just due to deficits in higher order aspects of cognition but also encompasses signifi- cant deficits in early sensory processing. NeuroReport 12:3815– 3820 & 2001 Lippincott Williams & Wilkins. Key words: Dorsal stream; Event-related potentials; ERP; High-density mapping; P1 component; Schizophrenia; VEP; Visual cortex; Visual evoked potential INTRODUCTION The neural mechanisms underlying cognitive dysfunction in schizophrenia remain to be fully elucidated. To date, a great deal of emphasis has been placed on dysfunction in higher-order regions of cortex such as prefrontal cortex [1,2] and medial temporal regions such as the hippocam- pus [3,4]. Similarly, electrophysiological investigations have largely concentrated on evidence for late processing deficits such as the well-known P300 deficits seen during cognitive tasks [5,6]. Recently, however, deficits at very early stages of sensory processing have been demonstrated in the auditory system of schizophrenia patients [7,8]. The implication from these findings is that cognitive impair- ment in schizophrenia is widespread and encompasses deficits in sensory processing as well as in higher order aspects of cognition. The current report investigates early sensory processing in the visual system. We focus on the P1 component of the visual evoked potential (VEP) as our dependent measure. P1 is an early scalp-recordable response to transiently presented visual stimuli, which peaks at 100 ms following stimulus onset and has been shown to arise from multiple generators in both the dorsal and ventral visual streams [9–12]. High- density electrical recordings allow for consideration of the dorsal and ventral contributions to the P1, which are best represented over parieto-occipital and occipito-temporal scalp respectively. P1 is followed by a negative deflection peaking at 160 ms, termed N1, which is localized more specifically over ventral visual stream structures such as the lateral occipital complex [13]. There is sufficient cause to predict early sensory proces- sing deficits in the visual system of schizophrenia patients. For example, schizophrenia patients show impairment in such basic visual functions as motion detection and smooth pursuit eye movements [14,15] and have shown consistent deficits on tasks such as velocity discrimination, coherent motion, spatial localization, backward masking, and lumi- nance contrast judgments [16–19]. It is of note that all of the above functions are associated with processing in the dorsal visual stream, suggesting that there may be impair- ment specific to the inputs to this stream. In support, a recent study has provided evidence that impairment is biased towards the magnocellular system [20] which pri- marily projects to the dorsal visual stream [21]. Butler et al. [20] showed that while steady-state visual evoked poten- tials (ssVEPs) were impaired for magnocellularly biased