Brain Advance Access published online on September 19, 2006
Brain, doi:10.1093/brain/awl233
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Department of Psychiatry, New York University School of Medicine, NY, USA; City College of the City University of New York, NY, USA
* To whom correspondence should be addressed. Visual processing deficits are an integral component of schizophrenia and are sensitive predictors of schizophrenic decompensation in healthy adults. The primate visual system consists of discrete subcortical magnocellular and parvocellular pathways, which project preferentially to dorsal and ventral cortical streams. Subcortical systems show differential stimulus sensitivity, while cortical systems, in turn, can be differentiated using surface potential analysis. The present study examined contributions of subcortical dysfunction to cortical processing deficits using high-density event-related potentials. Event-related potentials were recorded to stimuli biased towards the magnocellular system using low-contrast isolated checks in Experiment 1 and towards the magnocellular or parvocellular system using low versus high spatial frequency (HSF) sinusoidal gratings, respectively, in Experiment 2. The sample consisted of 23 patients with schizophrenia or schizoaffective disorder and 19 non-psychiatric volunteers of similar age. In Experiment 1, a large decrease in the P1 component of the visual event-related potential in response to magnocellular-biased isolated check stimuli was seen in patients compared with controls (F = 13.2, P = 0.001). Patients also showed decreased slope of the contrast response function over the magnocellular-selective contrast range compared with controls (t = 9.2, P = 0.04) indicating decreased signal amplification. In Experiment 2, C1 (F = 8.5, P = 0.007), P1 (F = 33.1, P < 0.001) and N1 (F = 60.8, P < 0.001) were reduced in amplitude to magnocellular-biased low spatial frequency (LSF) stimuli in patients with schizophrenia, but were intact to parvocellular-biased HSF stimuli, regardless of generator location. Source waveforms derived from inverse dipole modelling showed reduced P1 in Experiment 1 and reduced C1, P1 and N1 to LSF stimuli in Experiment 2, consistent with surface waveforms. These results indicate pervasive magnocellular dysfunction at the subcortical level that leads to secondary impairment in activation of cortical visual structures within dorsal and ventral stream visual pathways. Our finding of early visual dysfunction is consistent with and explanatory of classic literature showing subjective complaints of visual distortions and is consistent with early visual processing deficits reported in schizophrenia. Although deficits in visual processing have frequently been construed as resulting from failures of top-down processing, the present findings argue strongly for bottom-up rather than top-down dysfunction at least within the early visual pathway. Deficits in magnocellular processing in this task may reflect more general impairments in neuronal systems functioning, such as deficits in non-linear amplification and may thus represent an organizing principle for predicting neurocognitive dysfunction in schizophrenia.
Received May 10, 2006
Revised July 27, 2006
Accepted August 1, 2006
Article
Subcortical visual dysfunction in schizophrenia drives secondary cortical impairments
Pamela D. Butler 1 *, Antigona Martinez 2, John J. Foxe 3, Dongsoo Kim 2, Vance Zemon 4, Gail Silipo 2, Jeannette Mahoney 5, Marina Shpaner 3, Maria Jalbrzikowski 2, and Daniel C. Javitt 1
2 Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA
3 Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; City College of the City University of New York, NY, USA
4 Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA
5 Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA; Ferkauf Graduate School of Psychology, Yeshiva University, Bronx, NY, USA
Pamela D. Butler, E-mail: butler{at}nki.rfmh.org
Abstract 
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  D. Dickinson and P. D. Harvey Systemic Hypotheses for Generalized Cognitive Deficits in Schizophrenia: A New Take on An Old Problem Schizophr Bull, August 9, 2008; (2008) sbn097v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Martinez, S. A. Hillyard, E. C. Dias, D. J. Hagler Jr, P. D. Butler, D. N. Guilfoyle, M. Jalbrzikowski, G. Silipo, and D. C. Javitt Magnocellular Pathway Impairment in Schizophrenia: Evidence from Functional Magnetic Resonance Imaging J. Neurosci., July 23, 2008; 28(30): 7492 - 7500. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Wynn, J. Lee, W. P. Horan, and M. F. Green Using Event Related Potentials to Explore Stages of Facial Affect Recognition Deficits in Schizophrenia Schizophr Bull, July 1, 2008; 34(4): 679 - 687. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. I. Leitman, J. Loughead, D. H. Wolf, K. Ruparel, C. G. Kohler, M. A. Elliott, W. B. Bilker, R. E. Gur, and R. C. Gur Abnormal Superior Temporal Connectivity During Fear Perception in Schizophrenia Schizophr Bull, July 1, 2008; 34(4): 673 - 678. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. C. Skottun and J. Skoyles A few remarks on assessing magnocellular sensitivity in Schizophrenic patients Brain, November 1, 2007; 130(11): e83 - e83. [Full Text] [PDF]
|
|
|
|
|
|
P. D. Butler, A. Martinez, J. J. Foxe, D. Kim, V. Zemon, G. Silipo, J. Mahoney, M. Shpaner, M. Jalbrzikowskil, and D. C. Javitt Reply: A few remarks on assessing magnocellular sensitivity in patients with schizophrenia Brain, November 1, 2007; 130(11): e84 - e84. [Full Text] [PDF]
|
|