PMID- 14613674
OWN - NLM
STAT- MEDLINE
DCOM- 20040401
LR  - 20190917
IS  - 0920-9964 (Print)
IS  - 0920-9964 (Linking)
VI  - 64
IP  - 2-3
DP  - 2003 Nov 15
TI  - Magnocellular and parvocellular contributions to backward masking dysfunction in 
      schizophrenia.
PG  - 91-101
AB  - Patients with schizophrenia have repeatedly shown deficits in visual processing. 
      These deficits have been well documented using visual backward masking (VBM). The 
      VBM deficit in schizophrenia is thought to be due to aberrant interactions 
      between magnocellular (M) and parvocellular (P) visual pathways. To date, no 
      study has studied these claims with rigorous stimuli isolating M and P pathway 
      responses. This study examined the function of each pathway and their 
      interactions by creating M- and P-biased targets based on their known 
      physiological properties. The M system responds to very low luminance contrast 
      whereas the P system does not, and the P system responds to color contrast 
      whereas the M system generally does not. Thus, to activate the P system, target 
      letters and masks utilized color contrast, and to activate the M system, target 
      letters and masks utilized very low luminance contrast. Four conditions were 
      presented such that M- and P-biased targets were paired with both M- and P-biased 
      masks. A significant Group x Mask Condition interaction was found when a P target 
      was used in combination with an M or P mask, but not when an M target was used. 
      In particular, schizophrenia patients needed significantly longer interstimulus 
      intervals (ISIs) than controls to escape from masking in the P target/M mask 
      condition, but not in any of the other three conditions. In addition, the 
      critical stimulus durations (CSDs) for unmasked stimuli were significantly 
      increased for both M and P targets in patients relative to controls. These 
      findings demonstrate a significant impairment in M, but not P pathway, function 
      in patients with schizophrenia. Furthermore, deficits of letter identification, 
      including those of P targets, may also reflect impairment of the M pathway given 
      the priming function of the dorsal stream.
FAU - Schechter, Isaac
AU  - Schechter I
AD  - Program in Cognitive Neuroscience and Schizophrenia, Nathan Kline Institute for 
      Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA. 
      schechter@nki.rfmh.org
FAU - Butler, Pamela D
AU  - Butler PD
FAU - Silipo, Gail
AU  - Silipo G
FAU - Zemon, Vance
AU  - Zemon V
FAU - Javitt, Daniel C
AU  - Javitt DC
LA  - eng
GR  - R01 MH49334/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Schizophr Res
JT  - Schizophrenia research
JID - 8804207
SB  - IM
MH  - Adult
MH  - Attention/physiology
MH  - Color Perception/*physiology
MH  - Contrast Sensitivity/*physiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Neurons/physiology
MH  - Pattern Recognition, Visual/*physiology
MH  - Perceptual Masking/*physiology
MH  - Psychiatric Status Rating Scales
MH  - Reaction Time/physiology
MH  - Retina/physiopathology
MH  - Schizophrenia/diagnosis/*physiopathology
MH  - *Schizophrenic Psychology
MH  - Visual Cortex/physiopathology
MH  - Visual Pathways/*physiopathology
EDAT- 2003/11/14 05:00
MHDA- 2004/04/02 05:00
CRDT- 2003/11/14 05:00
PHST- 2003/11/14 05:00 [pubmed]
PHST- 2004/04/02 05:00 [medline]
PHST- 2003/11/14 05:00 [entrez]
AID - S0920996403000082 [pii]
AID - 10.1016/s0920-9964(03)00008-2 [doi]
PST - ppublish
SO  - Schizophr Res. 2003 Nov 15;64(2-3):91-101. doi: 10.1016/s0920-9964(03)00008-2.