Temporal dynamics, sensitivity and form discrimination in blindsight [Elektronische Ressource] / vorgelegt von Doerthe Seifert

Doerthe Seifert

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• Publié par: ludwig-maximilians-universitat_munchen
• Publié le: 01 janvier 2006
• Nombre de lectures: 14
• Langue: English
• Poids de l'ouvrage: 7 Mo

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Temporal dynamics, sensitivity and form
discrimination in blindsight
Doerthe Seifert










München 2006




























Temporal dynamics, sensitivity and form
discrimination in blindsight





Inaugural-Dissertation
zur Erlangung des
Doktorgrades der Philosophie an der
Ludwig-Maximilians-Universität
München


vorgelegt von
Doerthe Seifert
aus Hamburg


München, November 2006





























Referent: Prof. Dr. Hermann J. Müller
Korreferent: Prof. Dr. Thomas Stoffer
Tag der mündlichen Prüfung: 17.01.2007 Table of contents


Table of contents

Acknowledgements iii

CHAPTER I: 1
General Introduction

General definition of blindness 1

Residual visual capacities 3

Anatomy of visual system and blindsight 6

Typology of residual visual capacity 15

Training of the transition zone 21

Temporal dynamics 25

The aim of the study 31


CHAPTER II: 33
Classical blindsight experiment, control experiment and
tests of standardized methods (BIT and MWT-B)

Classical blindsight experiment 33

Control experiment 48

BIT 50

MWT-B 53


CHAPTER III: 55
The effects of flicker on discrimination performance in blindsight
Experiment 1: Discrimination of square-waved modulated gratings
of different orientations 61

Experiment 2: Discrimination of cosine-waved modulated gratings
of different orientations 74



Table of contents


CHAPTER IV: 88
The effects of flicker on detection performance in blindsight

Experiment 3: Detection of square-wave modulated continuous
or discontinuous gratings 89

Experiment 4: Detection of cosine-wave modulated continuous
or discontinuous gratings 93


CHAPTER V: 100
Temporal stimulation of transition zone

Patient RP, Results of Experiment 5 (a) 111

Patient RP, Results of Experiment 5 (b) 117

Patient FS, Results of Experiment 5 (a) 123

Patient FS, Results of Experiment 5 (b) 130

Patient FS, Results of Experiment 5 (c) 133

Patient LE, Results of Experiment 5 (a) 139

Appendix 153


References 157


Deutsche Zusammenfassung (German Summary) 166


Curriculum vitae 185

Acknowledgements


Acknowledgements

This dissertation was written at the Ludwig-Maximilians University in Munich
and supported by grant EL 248/3-1 from the German Research Foundation (DFG).
First of all, I would like to thank Prof. Dr. Hermann J. Müller for his support and
supervision of this thesis and for his possibility to work at his labour. Many thanks are
addressed to my supervisor Dr. Mark A. Elliott for his support, his help throughout all
stages of this work and that he inspired my interest in Experimental Psychology since
my first days as a student helper. His support enabled me to prepare conduct, analyse
and conclude the experimental work presented here. In addition, I would like to thank
all my colleagues for the nice time we shared together.
Special thanks go to my mother, Katharina Seifert, my father Kurt Seifert, my
sister, Anke Seifert, Franz-Josef Peine as well as to my aunt Erna Eberlein for their
endless support during my life and the past years. Last but certainly not least, I would
like to thank Frank to be able to stand to me during the single development stages of
this thesis.


Doerthe Seifert

Munich, November 2006




iii General Introduction

CHAPTER I:
General Introduction


General definition of blindness

Beside retinal blindness (by diverse optical diseases or damage to the retina) there
are forms of blindness arising due to damage to parts of the primary visual cortex (V1,
striatum, striate cortex or Brodmann area [BA] 17). These may arise due to stroke,
accident and neuronal degeneration, which can result in more or less impairment of
visual capacity and in the loss of parts of visual field. The generic term for this loss is
1
anopia . In terms of visual space and related to the dimensions and location (before or
after the optic chiasm) of the damaged tissue, visual field losses can be of different size:
from the restricted loss of a small area of visual field, which is referred to as scotoma,
up to quadrants (referred to as quadrantanopia), or even half fields (referred to as
hemianopia). Hemianopia can be homonymous (corresponding left or right visual field)
or heteronymous (bitemporal or binasal hemianopia), depending upon the exact location
of the lesion. Visual losses are located in the visual field contralateral to the site of the
lesion. Their dimensions can even extend to a complete visual field defect (and
therefore complete blindness) when brought about by large bilateral lesions to primary
area of occipital cortex.

1 Anopias = the inability to see, the totally or partially loss of vision, as in scotoma, quadrantenanopias
and hemianopias, ICD-10 H53.4.
1 Chapter I





Figure 1.1, upper depiction: Different kinds of anopias, affected by different lesions: white identifies the
intact (‘sighted’) and black the defect (‘blind’) visual field.
1. Left homonymous hemianopia: incomplete, incongruous, with macular splitting; 2. Bitemporal
hemianopia: heteronymous; 3. Right homonymous hemianopia (with macular sparing); 4. Compound
hemianopia: total left eye blindness plus right superior temporal quadrantanopia; 5. Central scotoma:
homonymous, congruous; 6. Left altitudinal hemianopia; 7. Quadrantanopia, homonymous right superior
temporal, congruous; 8. Binasal hemianopia: heteronymous (reproduced from Pietsch, P.).
lower depiction: Vision of a patient with hemianopia and a macular sparing (left reproduced from:
Arizona Center for the Blind and Visually Impaired (ACBVI); right reproduced from: Nova Vision.
Zentrum für Sehtherapie).

2 General Introduction

In general, the dimension of a scotoma can decrease from the edges to the centre
and in some cases that blind field can omit the centre of the visual field; this
2
phenomenon is referred to as macular sparing .


Residual visual capacities

Originally lesions to V1 were thought to cause irreversible and total blindness in
the affected parts of the visual field. However, in 1905 Bard reported that cortically
blind patients are able to locate a source of light (Bard, 1905, described in Stoerig, 1999
and Weiskrantz, 2004) and in 1917 Riddoch published a paper, in which he described
his examinations of a soldier who had suffered a gunshot wound, resulting in lesions to
3V1 (Fissura calcarina ) and thus to blindness in the affected parts of the visual field.
Riddoch found that his patient was able to detect motion (moving stimuli) within the
4
hemianopic field and was