May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Magnocellular and Parvocellular Contrast Sensitivity in Type 2 Diabetics With Normal Fundus and Non-Proliferative Retinopathy
Author Affiliations & Notes
  • M. Gualtieri
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
  • M. Bandeira
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
  • F. M. Damico
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
  • A. L. A. Moura
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
  • R. D. Hamer
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
    The Smith-Kettlewell Eye Research Institute, San Francisco, California
  • D. F. Ventura
    Neuroscience and Behavior, University of Sao Paulo, Sao Paulo, Brazil
  • Footnotes
    Commercial Relationships  M. Gualtieri, None; M. Bandeira, None; F.M. Damico, None; A.L.A. Moura, None; R.D. Hamer, None; D.F. Ventura, None.
  • Footnotes
    Support  FAPESP, CAPES, CNPq, FINEP IBN-Net
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 2896. doi:
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    • Get Citation

      M. Gualtieri, M. Bandeira, F. M. Damico, A. L. A. Moura, R. D. Hamer, D. F. Ventura; Magnocellular and Parvocellular Contrast Sensitivity in Type 2 Diabetics With Normal Fundus and Non-Proliferative Retinopathy. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2896.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To evaluate contrast sensitivity (CS) responses mediated by magnocelular (MC) and parvocellular (PC) systems in type 2 diabetics with normal fundus (NDR) and with non-proliferative retinopathy (DR).

Methods: : Pokorny & Smith’s (1997) steady/pulsed pedestal paradigms (SP/PP) were used to assess MC- and PC-dominated responses, respectively, in 27 NDR (13M; 56 ±11 yrs old; time of disease = 5 ± 4 yrs); 21 DR (6M; 58 ± 10 yrs old; time of disease = 9 ± 6 yrs) and 28 controls (CTRL) (11M, 44 ± 10 yrs old). The test consists of the presentation of an adaptation pedestal on which a luminance increment must be detected by the subject. Thresholds were measured with pedestals at 7, 12 and 19 cd/m2, and flash durations of 17 and 133 ms. Visual stimuli were generated by a 15-bit graphic board VSG 2/5 (CRS, Ltd) and presented on a Trinitron 21’ monitor GDM F500T9 (Sony). Tests were performed monocularly in a darkened room. For assessment of temporal features, we estimated critical durations (Tc) for each data set using the thresholds from two stimulus durations (Krauskopf & Mollon, 1971).

Results: : Both DR and NDR patients had significant reduction in CS in both SP and PP paradigms in relation to CTRL (Kruskal-Wallis test, p<0.0)1, implying losses in both MC and PC pathways. Responses from NDR and DR patients were elevated more as pedestal luminance increased. Tc’s were not significantly different from CTRL for either patient group, for either paradigm.

Conclusions: : Overall, DR and NDR diabetics had significant reduction of CS in both SP and PP paradigms, consistent with no preferential loss in either of the parallel processing pathways. The decrease in CS with luminance in both groups suggests impaired gain control system even in the absence of retinopathy. Our tests reveal no evidence of compromised processing speed in either diabetic group.

Keywords: diabetes • contrast sensitivity • visual impairment: neuro-ophthalmological disease 
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