Posts Tagged visual cortex

[ARTICLE] Reversing Hemianopia by Multisensory Training Under Anesthesia – Full Text

Hemianopia is characterized by blindness in one half of the visual field and is a common consequence of stroke and unilateral injury to the visual cortex. There are few effective rehabilitative strategies that can relieve it. Using the cat as an animal model of hemianopia, we found that blindness induced by lesions targeting all contiguous areas of the visual cortex could be rapidly reversed by a non-invasive, multisensory (auditory-visual) exposure procedure even while animals were anesthetized. Surprisingly few trials were required to reinstate vision in the previously blind hemisphere. That rehabilitation was possible under anesthesia indicates that the visuomotor behaviors commonly believed to be essential are not required for this recovery, nor are factors such as attention, motivation, reward, or the various other cognitive features that are generally thought to facilitate neuro-rehabilitative therapies.


Extensive damage to the visual cortex on one side of the brain produces blindness in the opposite hemifield (hemianopia) despite the sparing of other visual centers far from the site of the physical insult (Sand et al., 2013Goodwin, 2014). Of special note is the superior colliculus (SC), a midbrain structure that plays a major role in detecting, localizing, and orienting to visual targets. Its multisensory neurons allow it to use non-visual cues to facilitate this process (Stein and Meredith, 1993), and its location in the midbrain ensures that it is not directly damaged by a hemianopia-inducing cortical insult. Yet, as shown in the cat model of hemianopia, the loss of visual responses in the multisensory layers of the SC and the total absence of visual detection and orientation responses to contralateral visual stimuli following lesions of visual cortex reveal that it too is compromised, presumably via secondary excitotoxic injuries that may alter other input structures such as the basal ganglia (Jiang et al., 20092015). Interestingly, the dysfunction of SC appeared to be limited to its visual role. Its other sensory representations and sensorimotor roles remained intact: SC-mediated auditory and tactile detection and orientation responses were readily elicited (see also Sprague and Meikle, 1965).

Previously it was shown that hemianopia could be reversed using a non-invasive multisensory training paradigm (Jiang et al., 2015). The procedure consisted of presenting cross-modal combinations of spatiotemporally congruent auditory-visual cues in the blind hemifield of alert animals engaged in a sensory localization task. Because the animals were not deafened by the cortical lesion, they readily responded to the auditory-visual stimulus complex. After only a few weeks of daily multisensory training sessions, a striking change occurred: not only could the animals now detect and localize a visual stimulus throughout the previously blind hemifield, but they could also discriminate elementary visual patterns there. Visual responses that had been lost in the multisensory layers of the ipsilesional SC also returned, and cortico-SC circuits normally engaged in multisensory integration (i.e., projections from the anterior ectosylvian sulcus, AES) were found to be crucial for the recovery. The recovery could not be induced by training with visual or auditory cues alone. In an important series of studies in human patients, Làdavas and colleagues (Bolognini et al., 2005Leo et al., 2008Passamonti et al., 2009Dundon et al., 2015a,b) used a similar training paradigm and also met with success in evoking contralesional visual responses.

It is commonly believed that the success of this rehabilitative paradigm is a retraining of the visuomotor targeting behavior itself (see, review in Dundon et al., 2015a). In this case, the key factor would be the orienting action (initially elicited by the auditory stimulus) in the presence of the visual stimulus. Also, if true, it is reasonable to hypothesize that the effectiveness of this paradigm would be facilitated by other factors such as motivation, attention, arousal, and reinforcement, as these are commonly believed to enhance most neuro-rehabilitative therapies. An alternative explanation, however, is that the paradigm operates via the brain’s inherent mechanisms for multisensory plasticity, which operate independent of these factors and can be engaged under anesthesia (Yu et al., 2013). In this case, the requirement would only be repeated, reliable exposure to the visual-auditory stimulus complex in the blinded hemifield. The present study examined this possibility directly.

Materials and Methods

Adult mongrel cats (four male, three female) were obtained from a USDA-licensed commercial animal breeding facility (Liberty Labs, Waverly, NY, USA). The experimental procedures used were in compliance with the National Institutes of Health “Guide for the Care and Use of Laboratory Animals” (8th edition, NRC 2011) and approved by the Institutional Animal Care and Use Committee at Wake Forest School of Medicine. Each animal was first screened to ensure that it was tractable and responded to visual and auditory stimuli in both hemifields. All efforts were made to minimize the number of animals used.

Visual Detection and Orientation Testing

Visual orientation capabilities were quantitatively evaluated in a semicircular perimetry arena using previously described methods (see Jiang et al., 2015, see also Figure 1A). Animals were maintained at 80%–85% of body weight and obtained most of their daily food intake during, or immediately after, each behavioral session. Each animal was first trained to fixate directly ahead at a food reward held in forceps by one experimenter and protruded through a hole in the front wall of the apparatus 58 cm ahead at the 0° fixation point. Trial initiation was always contingent upon the animal establishing fixation. Once released by the animal handler (a second experimenter), the animal was required to move directly ahead to obtain the food reward. It was then trained to respond to the test stimulus (a white ping-pong ball at the end of a stick) presented at any 15° interval from 105° left to 105° right. This required little training as animals responded to the stimulus almost reflexively. Stimuli were presented manually and introduced suddenly from behind a black curtain while the animal was fixating. Additionally, on some trials, the ball remained hidden behind the opaque curtain and was tapped on the side of the apparatus to produce an auditory stimulus. If the animal oriented to and approached any test stimulus it was rewarded there, but could also move directly ahead to obtain a similar reward at the fixation point. The animal handler did not know the location of the upcoming test stimulus. This was determined by the experimenter holding the food reward, who also ensured that the trial did not begin if the animal had broken fixation. The verbal command “Go” triggered the release of the animal. “Catch trials” in which no stimulus was presented were interleaved with test trials at different locations to encourage the animal to minimize breaks in fixation, scanning movements, and “false” responses. Generally, in a given session, each of the 15° locations was tested at least 4–5 times. With few exceptions, the total number of trials/location was at least 100. The training criterion was an average of 95% correct responses. All animals reached criterion readily, had normal visual fields, and their weekly weight records revealed stable weight profiles.

Figure 1. The testing, training, and multisensory exposure paradigms. (A) Visual and auditory detection/localization capabilities were first assessed on both sides of space using a simple behavioral task. Cats were trained to fixate forward at 0° then orient to, and directly approach, a visual or auditory stimulus at any location in space. Visual stimuli were produced by lowering a ping pong ball below an obscuring curtain, and auditory stimuli were produced by tapping the ball against the apparatus wall while still obscured by the curtain. (B) Following surgery, a rehabilitation paradigm consisted of weekly sessions in which animals were exposed to cross-modal cues while anesthetized. As shown by the schematic at the lower left, the central LED (at 0°) of the display was briefly illuminated to signal the onset of the trial. It was followed by the combined LED-broadband noise burst at 45° in the contralesional hemifield. Traces illustrate the onset and duration of the stimuli. Panel (A) adapted from Jiang et al. (2015).

Continue —->  Frontiers | Reversing Hemianopia by Multisensory Training Under Anesthesia | Frontiers in Systems Neuroscience

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[Abstract] Interhemispheric visual competition after multisensory reversal of hemianopia


Unilateral lesions of visual cortex have the secondary consequence of suppressing visual circuits in the midbrain superior colliculus (SC), collectively producing blindness in contralesional space (“hemianopia”). Recent studies have demonstrated that SC visual responses and contralesional vision can be reinstated by a non‐invasive multisensory training procedure in which spatiotemporally concordant visual‐auditory pairs are repeatedly presented within the blind hemifield. Despite this recovery of visual responsiveness, the loss of visual cortex was expected to result in permanent deficits in that hemifield, especially when visual events in both hemifields compete for attention and access to the brain’s visuomotor circuitry. This was evaluated in the present study in a visual choice paradigm in which the two visual hemifields of recovered cats were simultaneously stimulated with equally‐valent visual targets. Surprisingly, the expected disparity was not found, and some animals even preferred stimuli presented in the previously blind hemifield. This preference persisted across multiple stimulus intensity levels and there was no indication that animals were less aware of cues in the previously blind hemifield than in its spared counterpart. Furthermore, when auditory cues were combined with visual cues, the enhanced performance they produced on a visual task was no greater in the normal than in the previously blind hemifield. These observations suggest that the multisensory rehabilitation paradigm revealed greater inherent visual information processing potential in the previously blind hemifield than was believed possible given the loss of visual cortex.


via Interhemispheric visual competition after multisensory reversal of hemianopia – Dakos – – European Journal of Neuroscience – Wiley Online Library

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[NEWS] Stroke: Rewiring eye-brain connection may restore vision

Many people who have a stroke also experience vision impairment as a result. New groundbreaking research looks at the mechanisms that play a role in this damage and shows that it may be reversible.

a person's eye looking up

New research may offer people who have lost some of their vision due to a stroke renewed hope that they may regain it.

A stroke can affect different parts of the brain. When it occurs in the primary visual cortex, which is the region of the brain that processes visual information, the lack of oxygenated blood can mean that the neurons (brain cells) active in that region incur damage.

In turn, this will affect people’s ability to see, and they may experience various degrees of vision loss. While some people who experience vision loss after a stroke may spontaneously regain their sight, most individuals do not.

So far, specialists have believed that damage to the primary visual cortex neurons causes a set of cells in the eye’s retina called “retinal ganglion cells” to become atrophied, meaning that they lose their ability to function.

When retinal ganglion cells become atrophied, it is highly unlikely that a person will ever recover sight in the affected area.

However, a new study, the findings of which appear in the journal Proceedings of the Royal Society B, has uncovered more information about the brain damage mechanisms relating to impaired eyesight.

“The integration of a number of cortical regions of the brain is necessary in order for visual information to be translated into a coherent visual representation of the world,” explains study co-author Dr. Bogachan Sahin, Ph.D., who is an assistant professor at the University of Rochester Medical Center in New York.

“And while the stroke may have disrupted the transmission of information from the visual center of the brain to higher order areas,” he adds, “these findings suggest that when the primary visual processing center of the brain remains intact and active, clinical approaches that harness the brain’s plasticity could lead to vision recovery.”

Therapies should ‘encourage neuroplasticity’

In the new study, the researchers worked with 15 participants who were receiving care at Strong Memorial and Rochester General Hospital for vision damage resulting from a stroke.

The participants agreed to take tests assessing their eyesight. They also had MRI scans to monitor their brain activity and an additional test that looked at the state of the retinal ganglion cells.

First, the investigators found that the health and survival of the retinal ganglion cells were highly dependent on activity in the associated primary visual area. Thus, the retinal cells connected to inactive brain areas would atrophy.

At the same time, however, the team surprisingly noted that some retinal cells in the eyes of people who had experienced vision impairment were still healthy and functional, even though the person had lost sight in that part of the eye.

This finding, the researchers explain, indicates that those healthy eye cells remained connected to fully active brain cells in the visual cortex. However, the neurons failed to correctly interpret the visual information that they received from the corresponding retinal ganglion cells, so the stimuli did not “translate” into sight.

“These findings suggest a treatment protocol that involves a visual field test and an eye exam to identify discordance between the visual deficit and retinal ganglion cell degeneration,” notes the study’s first author Dr. Colleen Schneider.

“This could identify areas of vision with intact connections between the eyes and the brain, and this information could be used to target visual retraining therapies to regions of the blind field of vision that are most likely to recover,” Dr. Schneider adds.

In the future, the researchers hope that their current discovery will allow specialists to fine-tune current therapeutic approaches or develop better strategies that will stimulate the damaged brain-eye connections to “rewire” correctly.

“This study breaks new ground by describing the cascade of processes that occur after a stroke in the visual center of the brain and how this ultimately leads to changes in the retina,” says senior author Brad Mahon, Ph.D.

By more precisely understanding which connections between the eye and brain remain intact after a stroke, we can begin to explore therapies that encourage neuroplasticity with the ultimate goal of restoring more vision in more patients.”

Brad Mahon, Ph.D.

via Stroke: Rewiring eye-brain connection may restore vision

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[WEB SITE] High-power prismatic devices may further expand visual fields for patients with hemianopia – ScienceDaily

Series of novel optical designs may address some limitations of existing prism technology, which can expand visual fields by up to 30 degrees

Summary: Three new eyeglasses have now been designedusing high-power prisms to optimally expand the visual fields of patients with hemianopia, a condition in which the visual fields of both eyes are cut by half. The new designs address some limitations of existing prism correction available to this population.

By embedding the current prism in a spectacle lens that has prismatic power in the opposite direction, the image shifting effect is increased by the summation of the power of both prism types. This design allows for up to 36 degrees of expansion to the visual field on the patient’s blind side. This design permits 5 degrees of scanning range to the blind side with full effect.
Credit: Massachusetts Eye and Ear

Researchers from the Schepens Eye Research Institute of Massachusetts Eye and Ear and Harvard Medical School have designed three new eyeglasses using high-power prisms to optimally expand the visual fields of patients with hemianopia, a condition in which the visual fields of both eyes are cut by half. The new designs, described in Optometry and Vision Science, address some limitations of existing prism correction available to this population.

Impairing either the left or right halves of the visual fields in both eyes, hemianopia affects more than one million Americans and is most commonly caused by stroke, brain tumors and head trauma. Hemianopia reduces the natural visual field of about 180 degrees to a mere 90 degrees. People with hemianopia have difficulty detecting hazards on their blind sides, leading to collisions, falls and other accidents. Patients with hemianopia cannot legally drive in Massachusetts, where a visual field of 120 degrees is required.

One method of treatment for hemianopia is to expand the visual field with prisms mounted on or embedded in eyeglasses. A research team led by Eli Peli, M.Sc., O.D., FAAO, Professor of Ophthalmology at Harvard Medical School and the Moakley Scholar in Aging Eye Research at the Schepens Eye Research Institute of Mass. Eye and Ear, has been developing prism devices to expand the visual field for these patients for more than 15 years. Their most recent commercially available device introduced in 2013, the peripheral prism glasses, has been shown to expand the visual fields of patients with hemianopia by as much as 30 degrees, optically shifting objects from the blind side of the visual field to the seeing side.

With the goal of expanding the visual field on the blind side even farther, the researchers explored new optical techniques to create higher power image shifting devices designed to bend the light farther than the 30-degree limit of conventional prisms. In conventional prisms, increasing the angle eventually results in the light bending back into the prism, trapped by what is called “total internal reflection.”

“It’s not just that we need a device with a higher angle of light shifting to let them see farther,” said Dr. Peli (pictured right). “We also want the new devices to provide the additional range of vision when the patient scans their eyes in both directions. The current prism devices support such flexibility only when scanning into the seeing side.”

The authors introduced three new high-power prism concept devices in the Optometry and Vision Science paper:

Yoked Prisms in the Carrier Lens

By embedding the current prism in a spectacle lens that has prismatic power in the opposite direction, the image shifting effect is increased by the summation of the power of both prism types. This design allows for up to 36 degrees of expansion to the visual field on the patient’s blind side. This design permits 5 degrees of scanning range to the blind side with full effect.

Bi-Part Double Fresnel Prism

To increase the power of the peripheral prism, the bi-part double Fresnel prism combines two prism segments angled to each other. This design allows for up to 43 degrees of expansion to the visual field on the patient’s blind side and an increase to 14 degrees scanning range into the blind side.

Mirror-Based Periscopic Prism

The third approach — not yet fully manufactured — uses a pair of angled mirrors to deflect the image from the blind side to the seeing side — not unlike prism correction. Due to the mirror-based design, this device is distortion-free and does not suffer from the color splitting effect of prisms, which reduces image clarity. It may allow for up to 40 degrees of expansion to the visual field on the patient’s blind side with much wider scanning range permitted.

The researchers intend to fully design and implement the mirror-based periscopic prism and also begin testing all three designs in patients with hemianopia.

“The new optical devices can improve the functionality of the current prism devices used for visual field expansion and may find use in various other field expansion applications such as a mobility aid for patients with tunnel vision,” Dr. Peli said.

Story Source:

Materials provided by Massachusetts Eye and Ear Infirmary. Note: Content may be edited for style and length.

Journal Reference:

Eli Peli, Alex R. Bowers, Karen Keeney, Jae-Hyun Jung. High-Power Prismatic Devices for Oblique Peripheral Prisms. Optometry and Vision Science, 2016; 93 (5): 521 DOI: 10.1097/OPX.0000000000000820

via High-power prismatic devices may further expand visual fields for patients with hemianopia: Series of novel optical designs may address some limitations of existing prism technology, which can expand visual fields by up to 30 degrees — ScienceDaily

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[ARTICLE] Adaptation, perceptual learning, and plasticity of brain functions – Full Text


The capacity for functional restitution after brain damage is quite different in the sensory and motor systems. This series of presentations highlights the potential for adaptation, plasticity, and perceptual learning from an interdisciplinary perspective. The chances for restitution in the primary visual cortex are limited. Some patterns of visual field loss and recovery after stroke are common, whereas others are impossible, which can be explained by the arrangement and plasticity of the cortical map. On the other hand, compensatory mechanisms are effective, can occur spontaneously, and can be enhanced by training. In contrast to the human visual system, the motor system is highly flexible. This is based on special relationships between perception and action and between cognition and action. In addition, the healthy adult brain can learn new functions, e.g. increasing resolution above the retinal one. The significance of these studies for rehabilitation after brain damage will be discussed.

Introduction by S. Trauzettel-Klosinski

This symposium highlighted the potential for learning and re-learning after visual and motor cortex lesions in the adult brain from an interdisciplinary perspective. We considered mechanisms such as adaptation, plasticity, and perceptual learning of different brain functions, as well as their applications for rehabilitation in patients with brain damage. Additionally, the potential for visual learning in the normal human brain was demonstrated.

In the visual system, the potential for recovery in the primary visual cortex is limited (part 1 by Jonathan Horton). Visual field defects caused by embolic stroke are constrained by the organization of the blood supply of the occipital lobe with respect to the retinotopic map. In terms of the arrangement and plasticity of the cortical map, it will be explained why some patterns of visual field loss and recovery following stroke are common, whereas others are essentially impossible. This is especially true along a visual field strip of constant width along the vertical meridian.

While the restitutive capacities of the primary visual cortex are limited, compensatory mechanisms can be very effective (part 2 by Susanne Trauzettel-Klosinski). They can occur spontaneously and can further be enhanced by training. In hemianopia, for example, fixational eye movements and scanning saccades can shift the visual field border towards the hemianopic side and improve spatial orientation and mobility.

In contrast to the visual system, the human motor system is highly flexible (part 3 by Theo Mulder). It is updated continuously by itself on the basis of sensory input and activity. The plasticity of the motor system is based on a special relationship between perception and action, as well as between cognition and action. New approaches to rehabilitation, for example by motor imagery, give an outlook on future possibilities.

Additionally, the healthy adult brain can learn new visual functions (part 4 by Manfred Fahle), for example the enhancement of resolution, which is higher than that of the retina. These functions, especially hyperacuity, can also be trained.

The authors will present a summary for each of the four talks.

Part 1: visual field recovery after lesions of the occipital lobe by Jonathan C. Horton

Recently, I attended a 60-year-old woman who had a spontaneous left parietal hemorrhage (Fig. 1). She underwent an emergency craniotomy to evacuate the hematoma. Her main deficit was a severe aphasia, which improved slowly. Once she regained sufficient ability to communicate, she complained about her vision on the right side. Her examination showed a total, macula-splitting right homonymous hemianopia. She has made nearly a complete recovery from her stroke, except for this devastating visual field cut. It has made reading a chore, forced her to give up driving, and will prevent her from returning to her job. This is a common scenario: after surviving a neurological disaster, patients discover that vision loss represents their most serious and enduring deficit. Why does central vision loss persist, and remain so stubbornly resistant to treatment?

Fig. 1 CT scan showing an acute left parietal hematoma, causing a right homonymous hemianopia. A CT scan performed 5 months later shows damage to the left optic radiations. The visual field cut never recovered

The answer lies in the organization of the visual pathway from eye to cortex. Retinal ganglion cell axons that are responsible for conscious perception project to the lateral geniculate nucleus. It serves as a relay station, boosting the information content of outgoing spikes compared with incoming spikes by integrating and filtering retinal signals [1]. Geniculate neurons send their projection to layer 4 of the primary visual cortex. Simply by crossing a single synapse in the thalamus, retinal output is conveyed directly to the primary visual cortex. In a sense, the retino-geniculo-cortical pathway is the aorta of our visual system (Fig. 2). After initial processing in the primary visual cortex, signals are analyzed in surrounding cortical areas that are specialized for different attributes, allowing us to perceive the images that impinge upon our retinae.

Fig. 2 Retinal input is conveyed to the primary (striate) cortex by a two-neuron chain, crossing a single relay in the lateral geniculate nucleus. Injury at any point cuts off visual perception, although a small projection (green shading) from the lateral geniculate to area MT allows “blindsight” in patients with homonymous hemianopia caused by a post-chiasmal lesion (pink shading). After Polyak (1957)

Continue —> Adaptation, perceptual learning, and plasticity of brain functions | SpringerLink

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[ARTICLE] Human blindsight is mediated by an intact geniculo- 2 extrastriate pathway – Full Text PDF


Although damage to the primary visual cortex (V1) causes hemianopia, many patients retain some residual vision; known as blindsight. We show that blindsight may be facilitated by an intact white-matter pathway between the lateral geniculate nucleus and motion area hMT+.

Visual psychophysics, diffusion-weighted magnetic resonance imaging and fibre tractography were applied in 17 patients with V1 damage acquired during adulthood and 9 age-matched controls. Individuals with V1 damage were subdivided into blindsight positive (preserved residual vision) and negative (no residual vision) according to psychophysical performance.

All blindsight positive individuals showed intact geniculo-hMT+ pathways, while this pathway was significantly impaired or not measurable in blindsight negative individuals. Two white matter pathways previously implicated in blindsight; (i) superior colliculus to hMT+ and (ii) between hMT+ in each hemisphere were not consistently present in blindsight positive cases. Understanding the visual pathways crucial for residual vision may direct future rehabilitation strategies for hemianopia patients.

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[ARTICLE] Electrical Stimulation of the Brain and the development of Cortical Visual Prostheses: An Historical Perspective – Full Text HTML/PDF


  • We revisit the discovery of visual cortex and of the brain’s electrical excitability.
  • We detail early experiences with electrical stimulation of visual cortex.
  • Subsequent attempts to develop a cortical visual prosthesis are explored.
  • We detail the development of technologies critical to current prosthesis designs.


Rapid advances are occurring in neural engineering, bionics and the brain-computer interface. These milestones have been underpinned by staggering advances in micro-electronics, computing, and wireless technology in the last three decades. Several cortically-based visual prosthetic devices are currently being developed, but pioneering advances with early implants were achieved by Brindley followed by Dobelle in the 1960s and 1970s. We have reviewed these discoveries within the historical context of the medical uses of electricity including attempts to cure blindness, the discovery of the visual cortex, and opportunities for cortex stimulation experiments during neurosurgery. Further advances were made possible with improvements in electrode design, greater understanding of cortical electrophysiology and miniaturization of electronic components. Human trials of a new generation of prototype cortical visual prostheses for the blind are imminent.


Advances in medicine, surgery and electronics have set the stage for a fusion of the physical and biological sciences; one in which prosthetic devices may restore lost functional capacity to the disabled. The emerging field of neuro-prosthetics embodies the totality of this integration, whereby sensory (Carlson et al., 2012, Guenther et al., 2012 and Weiland and Humayun, 2014), motor (Hochberg et al., 2012) and even cognitive (Hampson et al., 2012 and Hampson et al., 2013) deficits may be addressed. A significant share of the worldwide research effort in this regard is directed towards the development of visual prosthetics for the blind. Potential stimulation targets currently being investigated for visual prostheses include the retina (Chow et al., 2004, Dorn et al., 2013, Gerding et al., 2007 and Stingl et al., 2013), optic nerve (Brelen et al., 2010, Sakaguchi et al., 2009 and Wu et al., 2010), lateral geniculate body (Panetsos et al., 2011 and Pezaris and Eskandar, 2009) and the cerebral cortex (Brindley and Lewin, 1968b, Dobelle, 2000 and Schmidt et al., 1996). Human testing of implanted cortical electrode arrays for the evocation of visual percepts predates similar attempts at the retinal level by almost 30 years (Brindley and Lewin, 1968b, Humayun et al., 1996 and Humayun et al., 1999). Moreover, visual cortical prostheses offering limited functionality were chronically implanted in a number of patients throughout the 1970’s (Brindley, 1982, Dobelle et al., 1976 and Dobelle et al., 1979). Two retinal devices recently obtained regulatory approval in Europe (Argus II and Alpha IMS), with the Argus II also having obtained regulatory approval in the US (Weiland and Humayun, 2014). Cortical devices remain experimental only. Imminent human trials of a new generation of improved cortical devices render it timely to review the history of their development, including early electrical stimulation of human cerebral cortex and the first pioneering attempts to restore visual sensation to a profoundly blind person over 50 years ago.

Full Text HTML —> Electrical Stimulation of the Brain and the development of Cortical Visual Prostheses: An Historical Perspective

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[ARTICLE] Extrastriate visual cortex reorganizes despite sequential bilateral occipital stroke: implications for vision recovery – Full Text PDF

ABSTRACT (1304 characters without spaces)

The extent of visual cortex reorganization following injury remains controversial. We report serial functional magnetic resonance imaging (fMRI) data from a patient with sequential posterior circulation strokes occurring three weeks apart, compared with data from an agematched healthy control subject.

At 8 days following a left occipital stroke, contralesional visual cortical activation was within expected striate and extrastriate sites, comparable to that seen in controls. Despite a further infarct in the right (previously unaffected hemisphere), there was evolution of visual cortical reorganization progressed. In this patient, there was evidence of utilization of peri-infarct sites (right-sided) and recruitment of new activation sites in extrastriate cortices, including in the lateral middle and inferior temporal lobes. The changes over time corresponded topographically with the patient’s lesion site and its connections. Reorganization of the surviving visual cortex was demonstrated 8 days after the first stroke. Ongoing reorganization in extant cortex was demonstrated at the 6 month scan.

We present a summary of mechanisms of recovery following stroke relevant to the visual system. We conclude that mature primary visual cortex displays considerable plasticity and capacity to reorganize, associated with evolution of visual field deficits. We discuss these findings and their implications for therapy within the context of current concepts in visual compensatory and restorative therapies.

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A Systematic Approach to Visual System Neurorehabilitation — Population Receptive Field Analysis and Real-time Functional Magnetic Resonance Imaging Neurofeedback Methods – Full Text PDF

…How to approach visual neurorehabilitation?

To date, we have little understanding of how the visual cortex reorganizes after injury, and no proven effective treatment strategies to rehabilitate the recovery of visual perception in the affected portion of the visual field in V1-lesioned patients.

Understanding how to manipulate the brain’s capacity for plasticity is an important step in the long-term effort to design treatments aiming to enhance the ability of the nervous system to recover after injury. To make progress along this front, we need to:i) study the mechanisms by which the adult brain adapts and reorganizes after injury; and ii) devise approaches that will allow us to manipulate the process of reorganization to induce visual recovery.

The network of visual areas can be viewed as a heavily interconnected circuit subject to a series of hierarchy rules. Early areas usually process sensory information initially, by passing it on to higher areas, and in turn, extract “higher” order features and control the flow of information through feedback loops. Increased performance following training can therefore be the result of changes that occur in early areas (Schoups et al., 2001; Yotsumoto et al., 2008; Censor and Sagi, 2009; Karni and Sagi, 2008), or the result of changes that occur in “higher” visual areas and attentional networks (Law and Gold, 2008; Yang and Maunsell, 2004; Lewis et al., 2009).

Area V1 injuries, interrupt the cardinal feed-forward pathway but, as discussed above, visually driven information can still activate surviving extrastriate areas through bypassing routes (Cowey, 1974; Dineen et al., 1982; Rodman et al., 1989; Cowey and Stoerig, 1997; Baseler et al.,…


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