- •Visual Prosthetics
- •Preface
- •Acknowledgments
- •Contents
- •Contributors
- •1.1 The Visual System as an Engineering Compromise
- •1.2 An Overview of Human Visual System Architecture
- •1.2.1 Architecture and Basic Function of the Eye
- •1.2.2 Layout of the Retino-Cortical Pathway
- •1.2.3 Layout of the Subcortical Pathways
- •1.3 An Overview of Human Visual Function
- •1.3.1 Roles of Central (Foveal) Vision
- •1.3.2 Roles of Peripheral Vision
- •1.3.3 Roles of Dark-Adapted Vision
- •1.3.4 A Few Remarks Regarding Visual Development
- •1.4 Prospects for Prosthetic Vision Restoration
- •References
- •2.1 Introduction
- •2.2 Retina
- •2.2.1 Anatomy
- •2.2.2 Physiology and Receptive Fields
- •2.4.1 Anatomy
- •2.4.2 Physiology and Receptive Fields
- •2.6 The Role of Spatiotemporal Edges in Early Vision
- •2.7 The Role of Corners in Early Vision
- •2.7.1 Overview
- •2.8 Effects of Fixational Eye Movements in Early Visual Physiology and Perception
- •2.8.1 Overview
- •2.8.2 Neural Adaptation and Visual Fading
- •2.8.3 Microsaccades in Visual Physiology and Perception
- •References
- •3.1 Introduction
- •3.2 Background
- •3.3 Retinal Disease and Its Diversity
- •3.4 Retinal Remodeling
- •3.5 Retinal Circuitry
- •3.6 Retinal Circuitry Revision
- •3.7 Implications for Bionic Rescue
- •3.8 Implications for Biological Rescue
- •3.9 Final Remarks
- •References
- •4.1 Introduction
- •4.4 What Are the Limits to This Cortical Plasticity?
- •4.5 Possible Mechanisms Behind Brain Plasticity
- •4.6 Modulation of Brain Plasticity: Recent Developments
- •4.7 Neuroplasticity and Other Neuroprostheses Efforts
- •4.8 A Look at What Is Ahead
- •References
- •5.1 Introduction
- •5.2 Vision Changes Experienced by RP Patients
- •5.2.1 Overview
- •5.2.2 Visual Field Loss in RP
- •5.2.3 Changes in Color Vision and Glare Sensitivity in RP
- •5.2.4 Vision Fluctuations in RP
- •5.3 Visual Changes in Patients with Advanced Macular Degeneration
- •5.3.1 Changes Due to Wet AMD or Choroidal Neovascularization
- •5.3.2 Changes Due to Dry AMD or Geographic Atrophy
- •5.4 Charles Bonnet Syndrome
- •5.4.1 Overview
- •5.4.2 Complexity of Visual Hallucinations in CBS
- •5.4.3 Predictors and Alleviating Factors for CBS
- •5.5 Filling-In Phenomena (Perceptual Completion)
- •5.6 Remapping of Primary Visual Cortex in Patients with Central Scotomas from Macular Disease
- •5.7 The Preferred Retinal Locus for Fixation
- •5.8 Photopsias
- •5.8.1 Photopsias in RP
- •5.8.2 Photopsias in AMD and Other Ocular Diseases
- •5.9 Concluding Remarks
- •References
- •6.1 Introduction
- •6.2 Electrode–Electrolyte Interface
- •6.3 Electrode Material
- •6.3.1 Electrode Characterization
- •6.4 Overview of Electrode Materials for Neural Stimulation
- •6.5 Overview of Extracellular Stimulation
- •6.6 Safe Stimulation of Tissue
- •6.6.1 Mechanisms of Neural Injury
- •6.6.2 Parameters for Safe Stimulation
- •6.6.3 Stimulation Induced Injury in the Retina
- •References
- •7.1 Introduction
- •7.2 Power and Data Transmission
- •7.2.1 Wireline Connection
- •7.2.2 Inductive Coils
- •7.2.3 Serial Optical Telemetry
- •7.2.4 Photodiode Array-Based Prostheses
- •7.2.5 Thermal Safety Considerations
- •7.2.6 Conclusions: Comparing the Different Approaches
- •7.3 Tissue Response to a Subretinal Implant
- •7.3.1 Flat Implants
- •7.3.2 Chamber Implants
- •7.3.3 Pillar Arrays
- •7.4 Damage to Retinal Tissue from Electrical Stimulation
- •7.4.1 Effect of Pulse Duration
- •7.4.2 Electrode Size
- •7.5 Concluding Remarks
- •References
- •8.1 Introduction
- •8.2 Quasistatic Numerical Methods: The Admittance Method
- •8.2.1 Layered Retinal Model
- •8.2.2 Equivalent Electric Circuit
- •8.3 Three-Dimensional Activation Function Calculation
- •8.4 Safety of Implant
- •8.5 Conclusion
- •References
- •9.1 Pathophysiology of Retinal Degeneration
- •9.2.1 Outer Plexiform Layer
- •9.2.2 Inner Plexiform Layer
- •9.2.2.1 Bipolar Cell Excitation of Retinal Ganglion Cells
- •9.2.2.2 Amacrine Cell Modulation of Signal Processing
- •9.2.2.3 Inhibitory Transmitters
- •9.2.2.4 Acetylcholine and Dopamine
- •9.2.2.5 Neuropeptides
- •9.2.2.6 Putative neurotransmitters for retinal prosthesis
- •9.3 Neurophysiological Changes in Retinal Degeneration
- •9.4 Rationale for a Neurotransmitter-Based Retinal Prosthesis
- •9.4.1 Limitations of Electrical Stimulation
- •9.5 Technical Considerations and Design Approaches
- •9.5.1 Operating Principles for a Neurotransmitter-Based Retinal Prosthesis
- •9.5.2 Establishing a Retinal Prosthesis/Synaptic Interface
- •9.5.2.1 The Proximity Requirement
- •9.5.2.2 Convective Delivery of Neurotransmitters Via Microfluidics
- •9.5.2.3 Functionalized Surfaces for Neurotransmitter Stimulation
- •9.5.2.4 Synaptic Requirements for l-Glutamate Mediated Neuronal Stimulation
- •9.6 Summary
- •References
- •10.1 Introduction
- •10.2 Pioneering Experiments
- •10.2.1 Stimulation with No Chromophores
- •10.2.2 Azo Chromophores
- •10.3 Current Research
- •10.3.1 Caged Neurotransmitters
- •10.3.2 Pore Blocker and Photoisomerization
- •10.3.3 The Channelrhodopsins
- •10.3.4 Melanopsin
- •10.4 Synthetic Chromophores and Artificial Sight
- •References
- •11.1 Background
- •11.2 Physical Structure of Intracortical Electrodes
- •11.3 Charge Injection Using Intracortical Electrodes
- •11.3.1 The Intracortical Electrode as a Transducer
- •11.3.2 Charge Injection Limits
- •11.4 Intracortical Electrode Coatings
- •11.5 Characterization of Intracortical Electrodes
- •11.5.1 Cyclic Voltammetry
- •11.5.2 Electrode Stimulation Voltage Waveforms
- •11.5.3 Non-ideal Access Resistance Behavior
- •11.5.4 Non-linear Electrode Polarization
- •11.5.5 Determining Electrode Safety
- •11.6 Contrasts of In Vitro and In Vivo Behavior
- •11.7 Alternative Coatings for Improving Intracortical Electrodes
- •11.7.1 SIROF
- •11.7.2 PEDOT
- •11.7.3 Carbon Nanotube Coatings
- •11.8 Conclusion
- •References
- •12.1 Introduction
- •12.2 Responses of RGCs to Electrical Stimulation in Normal Retina
- •12.2.1 Epiretinal Stimulation
- •12.2.1.1 Target of Stimulation
- •12.2.1.2 The Site of Spike Initiation in RGCs
- •12.2.1.3 Threshold vs. Stimulating Electrode Diameter
- •12.2.1.4 Spatial Extent of Activation
- •12.2.1.5 Selective Activation
- •12.2.1.6 Temporal Response Properties
- •12.2.2 Subretinal Stimulation
- •12.2.2.1 Target of Stimulation
- •12.2.2.2 Threshold vs. Polarity of Stimulation Pulse
- •12.2.2.3 Spatial Extent of Activation
- •12.2.2.4 Temporal Response Properties
- •12.2.2.5 Dynamics of the Retinal Response
- •12.4 Responses of RGCs to Electrical Stimulation in Degenerate Retina
- •12.4.1 Epiretinal Stimulation
- •12.4.2 Subretinal Stimulation
- •12.4.2.1 Response Properties of RGCs
- •12.4.2.2 Activation Thresholds of RGCs
- •12.5 Cortical Responses to Retinal Stimulation
- •12.5.1 Spatial Properties Revealed by Cortical Measurements
- •12.5.2 Local Field Potentials
- •12.5.3 Elicited Responses Are Focal
- •12.5.4 Cortical Measurements Reveal Electrode Interactions
- •12.5.5 Temporal Responsiveness in Cortex
- •12.6 Suggestions for Future Studies
- •References
- •13.1 Introduction
- •13.2 General Considerations for Acute Retinal Stimulation Experiments
- •13.3 Surgical Technique
- •13.4 Threshold Measurements
- •13.5 Spatial Resolution and Pattern Perception
- •13.6 Temporal Resolution
- •13.7 Subretinal Versus Epiretinal Stimulation
- •13.8 Less Invasive Stimulation Procedures
- •13.9 Conclusions and Outlook
- •References
- •14.1 Introduction
- •14.2 Overview of Chronic Retinal Implant Technologies
- •14.2.1 The Retinal Implant AG Microphotodiode Prosthesis
- •14.2.2 The Intelligent Retinal Implant System
- •14.2.3 Second Sight Medical Products, Inc. A16 System
- •14.3 Thresholds on Individual Electrodes
- •14.3.1 Single Pulse Thresholds Using the SSMP System
- •14.3.2 Pulse Train Integration and Temporal Sensitivity
- •14.4 Suprathreshold Brightness
- •14.4.1 Brightness Using the Retinal Implant AG System
- •14.4.2 Brightness Using the Intelligent Medical Implant System
- •14.4.3 Brightness Using the SSMP A16 System
- •14.5 Spatial Vision
- •14.5.1 Spatial Vision with the Retinal Implant AG System
- •14.5.2 Spatial Vision with the Intelligent Medical Implant System
- •14.5.3 Spatial Vision with the SSMP A16 System
- •14.6 Models to Guide Electrical Stimulation Protocols
- •14.7 Conclusions
- •References
- •15.1 Background
- •15.2 Cortical Surface Stimulation
- •15.3 Intracortical Microstimulation
- •15.4 Optic Nerve Stimulation
- •15.5 What Is Known and What Needs to Be Done
- •15.6 Current Research Efforts
- •15.6.1 Optic Nerve Stimulation
- •15.6.2 Cortical Surface Stimulation
- •15.6.3 Intracortical Stimulation of Visual Cortex
- •15.6.4 CORTIVIS Program
- •15.6.5 Lateral Geniculate Stimulation
- •15.7 Microelectrode Arrays and Stimulation Hardware
- •15.7.1 Miniature Cameras
- •15.7.2 Animal Models
- •15.7.3 Image Processing and Phosphene Mapping
- •15.8 Conclusion
- •References
- •16.1 Introduction
- •16.2 Simulation Techniques and Basic Parameters
- •16.2.1 Gaze Tracking and Image Stabilization
- •16.2.2 Filter Engine Parameters
- •16.2.2.1 Raster Spatial Properties
- •16.2.2.2 Dot Spatial Properties
- •16.2.2.3 Temporal Properties
- •16.2.2.4 Dynamic Background Noise
- •16.2.2.5 Input Filtering/Windowing, Image Enhancement
- •16.3 Optotype Resolution and Reading
- •16.3.1 Visual Acuity
- •16.3.2 Reading
- •16.4 Face and Object Recognition
- •16.5 Visually Guided Behavior
- •16.5.1 Hand–Eye Coordination
- •16.5.2 Wayfinding
- •16.6 Visual Tracking
- •16.7 Computational Simulations
- •16.8 Conclusion
- •References
- •17.1 Introduction
- •17.2 Situating Image Analysis
- •17.3 The Experimental Framework
- •17.4 Tracking a Low-Resolution Target
- •17.5 Discussion
- •17.6 Conclusion
- •References
- •18.1 Introduction
- •18.2 Representation of Visual Space on the Visual Cortex
- •18.3 Cortical Stimulation Studies
- •18.4 Variability in Occipital Cortex
- •18.5 Phosphene Map Estimation
- •18.6 Psychophysical Studies with the Estimated Maps
- •References
- •19.1 Importance of Mapping
- •19.3 The Computer Era: Refining the Pointing Method of Phosphene Mapping
- •19.4 Verbal Mapping
- •19.5 Mapping Studies Using Subject Drawings
- •19.6 Recent Simulation Studies Using Phosphene Mapping
- •19.6.1 Tactile Simulations at Shanghai Jiao Tong University
- •19.6.2 Simulations in Our Laboratory
- •19.7 Concluding Remarks on Phosphene Mapping Techniques
- •References
- •20.1 Introduction
- •20.2 Principles for Assessment of Prosthetic Vision
- •20.2.1 Experimental Design
- •20.2.2 The Importance of Pre-operative Testing
- •20.2.3 Post-operative Assessment
- •20.2.4.1 Potential Approaches
- •20.2.4.2 Avoidance of Bias
- •20.2.4.3 Criteria for Sound Testing
- •20.2.4.4 Forced Choice Procedures
- •20.2.4.5 Response Time
- •20.2.4.6 Task (Perceptual) Learning
- •20.2.4.7 Establishing Criteria for Meaningful Change
- •20.2.4.8 Light Level
- •20.3 Vision Assessment in Prosthesis Recipients: Overview
- •20.3.1 Visual Function Assessment: Overview
- •20.3.2 Visual Performance Assessment: Overview
- •20.3.2.1 Measured Visual Performance
- •20.3.2.2 Self-Reported Visual Performance
- •20.4 Visual Function Assessment
- •20.4.1 Candidate Measures
- •20.4.1.1 Contrast Sensitivity (Contrast Detection)
- •20.4.1.2 Contrast Discrimination
- •20.4.1.3 Motion Perception
- •20.4.1.4 Depth Perception
- •20.4.2 Tests Used in Prosthesis Trials
- •20.4.3 Tests that Have Been Designed for Use with Prostheses
- •20.4.4 Vision Tests for Very Low Vision
- •20.5 Visual Performance Assessment
- •20.5.1 Measured Performance
- •20.5.2 Self-Reported Performance (Questionnaires)
- •20.6 Summary
- •References
- •21.1 Concepts of Functional Vision and Rehabilitation
- •21.1.1 Application to Orientation and Mobility
- •21.1.2 Application for Activities of Daily Living
- •21.1.3 Patient Lifestyle and Expectations
- •21.1.4 Congenital and Adventitious Vision Loss
- •21.2 Evaluation and Intervention with Prosthetic Vision
- •21.2.1 Evaluation
- •21.2.2 Intervention
- •21.3 Measuring Functional Outcomes
- •21.4 The Future
- •References
- •Author Index
- •Subject Index
19 Phosphene Mapping Techniques for Visual Prostheses |
373 |
19.4 Verbal Mapping
Though mapping of phosphenes by retinal and optic nerve stimulation was reported long after the first cortically evoked phosphenes were characterized, the methods used were not very different. Several papers by Humayun et al. mention mapping of retinally evoked phosphenes [18–20], but they do not provide detailed information about mapping conditions, such as gaze-control of the subject or tactile references. In acute experiments Humayun et al. constructed absolute maps by asking the subject to verbally inform the experimenter of the quadrant (1–4), or clock hour (e.g., “9 o’clock”) in which the phosphene was perceived [18]. As expected, the results confirmed that subjective phosphene location corresponded well with the electrically stimulated area on the retina. On the basis of these findings, they extended their observations to relative measures by providing simple patterns through multi-electrode probes on the retinal surface and asking the subject about their percepts in acute experiments [19].
Verbal mapping was also applied in a study using TMS to evoke phosphenes in sighted subjects [27]. Subjects were placed in a darkened room with eyes closed to facilitate phosphene percepts elicited by stimulation of the occipital lobes. Subjects reported if the phosphenes appeared in the upper or lower visual field, and whether the percepts were centrally or peripherally located. It appeared that peripheral phosphenes were encountered more often than central ones. Furthermore, phosphenes were more often observed in the lower-field than in the upper field. The first finding is unexpected, since the central visual field at the occipital pole (i.e. the foveal projection) is more accessible for TMS than the peripheral retinal projections located at more rostral aspects from the calcarine fissure. The authors speculated that TMS in this study may have activated peristriate cortical areas.
Fernandez et al. [14] proposed an alternative method of phosphene imaging by verbal communication for sighted people. This method incorporates several training phases by using a clock-face division of visual space. Each of the 12 sectors is labeled accordingly and divided into annuli to produce an inner, middle, and outer portion, representing displacement between the fovea and visual periphery. In the training phase subjects are provided with a computer screen and learn to specify the projection of a light spot over the clock-face frame. Initially, spots of light are presented onto a full outline of the frame and subjects are asked to indicate in which of the 36 sections the spot appears (hour and eccentricity). The second training phase is performed without sector labeling and subjects receive feedback about their performance. The last phase consists of phosphene localization without the frame and subjects again receive feedback on their performance. Each of the training phases are repeated until the subject achieves a required percentage correct performance level, before proceeding to the next phase. After training, testing consists of identification of the location of phosphenes in an imaginary frame. The authors predict that this method should be faster and should yield a higher spatial resolution and more discrete responses from the subjects than other absolute mapping methods. In addition, any effects of visuo-motor transformations required for drawing are eliminated by this method.
374 |
H.C. Stronks and G. Dagnelie |
The authors mention that blind people could learn this method (though training with a visible frame would be impossible) with the help of a dartboard divided into 12 sectors and three annuli, much like the method of Mladejovsky et al. [26] discussed above.
19.5 Mapping Studies Using Subject Drawings
After their first studies on phosphene mapping using acute retinal stimulation (Sect. 19.3), Humayun et al. chronically implanted a retinitis pigmentosa patient without functional vision with a 16-electrode retinal implant [20]. They mapped the phosphenes by letting the subject draw the percepts on a drawing board positioned on the subject’s lap. Similar to their preceding studies using verbal information discussed above, the constructed phosphene maps indicated that percepts correspond well with the retinal layout; i.e., electrodes temporally located evoked nasally perceived phosphenes (and vice versa), and superiorly located electrodes evoke inferiorly perceived phosphenes (and vice versa). Resolution appeared to be 1.5° of visual angle.
In another study a very similar drawing method was used to map phosphenes of sighted subjects with intractable epilepsy who were chronically implanted with subdural electrodes in the extrastriate visual cortex [21]. Subjects were asked to look at the center of a white board positioned 2 m away. The white board was divided into sections by horizontal and vertical median lines. The subjects were instructed to make drawings on a white paper, regarding the outline and location of the phosphenes. The paper was one tenth the size of the white board and had similar dividing lines. Phosphene shape, color and motion were also recorded. These drawings were then used to extract polar angle and eccentricity of the phosphene for mapping purposes. The results of this study showed that retinotopic maps could also be found on the lateral occipital cortex.
Several TMS studies made use of drawings of phosphenes made by subjects, starting with an early study by Marg and Rudiak using normally sighted people [24]. For optimal phosphene perception, subjects were seated in a darkened room with their eyes closed. Subjects made drawings of the phosphenes and reported on characteristics such as the shape, color, brightness/vividness and position and distance in the visual field relative to the fixation point. Besides detailed morphology of TMS-evoked phosphenes, the authors reported that phosphenes in the peripheral field of vision occur more frequently than central ones, in agreement with the findings of Ray et al. [27].
Subject drawings of perceived phosphenes were also applied in a TMS study with sighted subjects and two visually impaired subjects. One of the visually impaired subjects lost all functional vision at the age of 53 (subject was 61 years of age at the time of testing), while the other had a partial vision loss due to severe damage to the left striate cortex at the age of 8 (subject was in his early 40s when testing took place) [5]. Phosphenes were mapped by letting the subjects
