Archive for category Hemianopsia

[VIDEO] Visual Field Examination – YouTube

Basic defects of Visual field. Common Findings: Right Hemianopia, Left Hemianopia, Bitemporal Hemianopia , Tunnel vision.

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[BLOG POST] Traumatic Brain Injury- Virtual Reality Technology Used For Vision Therapy

February 12, 2018

So, here is a new subject that hints at hope for traumatic brain injury (TBI) patients. I have previously discussed the role of vision therapy in helping head injury patients, especially those who are having difficulty reading.
Vision therapy is a set of vision exercises and training performed by optometrists with unique equipment in their offices.

Vision therapy certainly has a role in rehabilitation but has numerous obstacles. Number one- patients must make regular appointments for a doctor’s office visit often located some distance from home. Two, only a few optometrist’s perform vision therapy. And third, the cost of therapy is usually not covered by medical insurance.

The future may lie in VIRTUAL REALITY– futuristic-looking goggles and head sets that allow individuals to play 3-D computer games in an immersive environment. The technology keeps improving and costs are coming down.

Forward-looking technology companies are also developing programs for traumatic brain injury (TBI) patients. Only early versions are currently available but the possibility of at-home rehabilitation will soon become a medical reality. All of medicine is moving in this direction.

Reading, depth perception, contrast sensitivity, and peripheral vision disorders can all be explored in virtual reality. The brain and the eye will truly come together in a revolution of new products to aid patients with ocular disease. There are already devices to help people who are blind, but the cost of such devices is considerable. The cost of virtual reality computer goggles and headsets will be coming down in price to sell to the general public- the same techniques that are being explored to develop entertainment are being developed by health companies to treat patients.

In the next year or two, the market will present these devices and an at-home device and therapy to treat TBI victims will be available. In my blog I have explained the many ways head injury can effect eyesight, but there are almost no cures. Cures may be a long way off, but programs to help people read again, reduce double vision, and regain their ability to judge depth are already in the pipeline. I’m not currently an investor in any device, and I will not discuss specific companies, but the research and data is on the internet.

Also, there are already programs you can get on a regular computer screen for vision training and I will discuss these in future blogs. Again, ophthalmologists interested in TBI and related visual disorders can be at a frontier of a whole new branch of ophthalmology. I examine and evaluate TBI patients in my practice everyday and I will keep those who read my blog posted on new information.

Stay tuned!

Steven H. Rauchman, M.D. is an eye physician and surgeon who has been in private practice for 30 years. He has served as an Traumatic Brain Injury (TBI) medical/legal expert for the last 6 years specializing in the area of personal injury and related traumatic brain injuries.


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[ARTICLE] Enhancing visual performance in individuals with cortical visual impairment (homonymous hemianopsia): Tapping into blindsight – Full Text


Patients with occipital lobe damage may have blind areas in their visual field.

Other non-cortical areas of the brain still process visual information.

Modifying visual input can stimulate non-cortical visual processing areas.

Augmented virtual reality goggles as a therapy for cortical blindness is proposed.


Homonymous hemianopsia is a type of cortical blindness in which vision is lost completely or partially in the left half or the right half of the field of vision. It is prevalent in approximately 12% of traumatic brain injury and 35% of strokes. Patients often experience difficulty with activities such as ambulating, eating, reading, and driving. Due to the high prevalence of homonymous hemianopsia and its associated difficulties, it is imperative to find methods for visual rehabilitation in this condition. Traditional methods such as prism glasses can cause visual confusion and result in patient noncompliance. There is a large unmet medical need for improving this condition. In this article, we propose that modifying visual stimuli to activate non-cortical areas of visual processing, such as lateral geniculate nucleus and superior colliculus, may result in increased visual awareness. Presenting high contrast and low spatial frequency visual stimuli can increase visual detection in patients with cortical blindness, a phenomenon known as blindsight. Augmented virtual reality goggles have the potential to alter real-time visual input to high contrast and low spatial frequency images, possibly improving visual detection in the blind hemifield and providing an alternative therapy for homonymous hemianopsia.

Graphical abstract


Cortical visual impairment comprises a significant component of strokes and traumatic brain injury. Cortical visual impairment includes homonymous hemianopsia, in which vision is lost completely or partially in the left half or the right half of the field of vision. Homonymous hemianopsia is prevalent in approximately 12% of traumatic brain injury and 35% of strokes [1–3]. Individuals with this vision loss usually have difficulties with activities of daily living such as ambulating, eating, reading, and driving [4,5]. Due to the high prevalence of homonymous hemianopsia and its associated difficulties, it is imperative to find methods for visual rehabilitation in this condition. Traditional methods of visual rehabilitation for homonymous hemianopsia include fitting spectacles with prisms to shift the visual field from the blind hemifield to the intact visual field. This is accomplished by placing the base of the prism in the blind hemifield, which shifts the image toward the apex of the prism into the intact hemifield. Many patients discontinue treatment with prisms because the prisms may induce visual confusion and double vision [1–4]. Another technique used is to train individuals with hemianopsia to make quick eye movements in the direction of the blind hemifield, though there is not much evidence supporting efficacy [6]. Although these methods may provide some compensation for the visual field loss, they do not restore the impaired visual field. Accordingly, other methods of improving vision are needed.

Individuals with homonymous hemianopsia do not consciously see vision in the blind hemifield. However, there is evidence of a ‘blindsight’ phenomenon, whereby some affected individuals can detect objects in their blind visual field, albeit without conscious awareness of being able to see the object. Functional magnetic resonance imaging (fMRI) studies have indicated that visual processing occurs in other parts of the brain, such as the lateral geniculate nucleus (LGN) and superior colliculus (SC) (Fig. 1). Visual processing in these regions provides the neural network that enables patients with blindsight to see [7–11]. Blindsight has been manipulated in some individuals to enhance visual awareness. Sahraie et al. studied a patient with homonymous hemianopsia and well-documented blindsight over a long period of time [7]. The patient reported increased awareness of visual stimuli in his blind visual field when the stimulus was presented with high contrast and low spatial frequency. Spatial frequency refers to the level of detail in an image appearing within a degree of the visual field. Temporal frequency, the number of times a stimulus is flashed within a second, also modulates detection. Multiple studies have shown that within a temporal frequency range of 5–20 Hz (cycles/s), detection of visual stimuli in a forced-choice test is significantly better than chance [7–11]. The time of stimulus onset also affects the rate of detection. Patients with parietal lobe injury often cannot detect a visual stimulus in the neglected hemifield when it is presented simultaneously in the intact hemifield, but can detect the stimulus when it is presented by itself in the neglected hemifield only, a phenomenon known as visual extinction [12,13]. It is thought that visual extinction reflects an attentional deficit as opposed to primarily a sensory deficit, although this remains an area of active research [14]. Despite that visual extinction is primarily studied in patients with hemi-neglect, patients with hemianopsia also can have hemi-neglect from injury to both the occipital and parietal lobes [15]. Therefore, the relevant visual variables for increasing visual detection in hemianopsia are stimuli contrast, spatial frequency, temporal frequency and stimulus onset asynchrony.


Figure 1. 3-D representation of tracts overlaid on T1-weighted fMRI images between the lateral geniculate nucleus (LGN) and human motion complex (hMT+), adapted from Ajina and colleagues (eLife. 2015;4:e08935. doi: 10.7554/eLife.08935[26]. (A) Dark green tracts are in the ipsilesional hemisphere, light green tracts are in the contralesional hemisphere and in controls. (B) Fractional anisotropy, reflecting neuronal damage, demonstrates increased impaired tissue microstructure in the ipsilesional tract in blindsight negative patients as compared with blindsight positive patients and controls.


Continue —>  Enhancing visual performance in individuals with cortical visual impairment (homonymous hemianopsia): Tapping into blindsight – ScienceDirect

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[WEB SITE] Homonymous hemianopsia: Causes, symptoms, diagnosis, treatment, prevention, and prognosis

homonymousWhat homonymous hemianopsia (HH) can be defined as is when an individual is reduced to only being able to see one side of the visual world from each eye. HH is commonly caused by a stroke and will cause a person to bump into objects or fail to see objects or people. It is the brain that is the issue in homonymous hemianopsia, rather than the eyes themselves. When the left side of the brain is injured, there is loss to the right half of the visual world of each eye. An injury to the right brain could potentially cause a loss to the left half of the visual world of each eye.

Causes of homonymous hemianopsia

Although homonymous hemianopsia can be congenital (present from birth), the primary cause in approximately 52 to 70 percent of adult cases is a stroke. About eight to 10 percent of stroke victims have homonymous hemianopsia. Other leading causes of homonymous hemianopsia include brain injury (14 percent of cases) and tumors (11 percent). Legions from the optic tract to the visual cortex can be the cause of homonymous hemianopsia.

Other conditions that can cause homonymous hemianopsia include Alzheimer’s disease; arteriovenous malformation; cortical basal ganglion degeneration;Creutzfeldt–Jakob disease; epilepsy; lymphoma, mitochondrial encephalomyopathy;Multiple sclerosis; and vertebrobasilar dolichoectasia.

Symptoms of homonymous hemianopsia

The main symptom that arises due to homonymous hemianopsia is the experience of bumping or running into things on the side that is visually defective. It should be made clear that the condition makes those afflicted perceive a full field of vision, but in reality, information about half of their visual field isn’t being seen.

Activities such as crossing the street or driving can become fatal due to the loss of vision from oncoming traffic. Objects on one side might go unseen, such as half a plate of food being uneaten.

For those with left homonymous hemianopsia, reading will be difficult, as it will be hard to find the start of next line. Those with right homonymous hemianopsia will find reading takes a lot longer, since we read from left to right.

Visual hallucinations are a common symptom of homonymous hemianopsia. Hallucinations can take the form of recognizable objects, or they can be unformed lights, shapes, or geometric figures.

How to diagnose homonymous hemianopsia

A visual field acuity test, also known as a perimetry test, is necessary in order to diagnose homonymous hemianopsia. In this test, the patient responds to a series of flashing lights while focusing on a target. A visual field test creates a printout of the light threshold perceptible to a patient.

Your eyes may also be checked to see if the retina, macula, and optic nerve are healthy and not causing problems.

An MRI of the brain can diagnose the location of a brain injury that may be causing homonymous hemianopsia.

How to treat homonymous hemianopsia

Treatment for homonymous hemianopsia involves improving the ability to read and navigate the environment.

To improve reading, a straight edge can be used to help direct eyes to the next line of text. Another strategy is to condition the ability to capture each word within the field of vision. Additionally, text can be held at a 45- to 90-degree angle in order to read vertically; those with right hemianopsia can read down and those with left hemianopsia can read up.

Improving the ability to navigate the environment can be done by reconditioning visual habits. Eyes should be directed towards the good visual field when walking. In a new environment, a person should stop, scan from side to side, and see where objects and people are located, then picture this in the brain. Performing word and picture search puzzles can help improve the ability of the eyes to scan at close range.

If homonymous hemianopsia is caused by an underlying disorder, other treatments will be applied.

Prevention and prognosis of homonymous hemianopsia

Prevention of homonymous hemianopsia cannot be completely guaranteed with any methods. However, since homonymous hemianopsia’s main cause is a stroke, following guidelines to prevent having a stroke (lower blood pressure, lose weight, exercise more, moderate drinking, quit smoking) is an effective strategy to avoid experiencing homonymous hemianopsia.

The prognosis for homonymous hemianopsia hinges on the condition’s cause and severity of the brain injury. A severe brain injury does not have a good likelihood of complete recovery.

Total recovery of homonymous hemianopsia occurs within four weeks in 17 to 19 percent of those who experience symptoms due to a stroke. Some studies point to 55 percent of patients having some improvement within four weeks and all other improvement taking place in a 12–18-month period after the stroke.

If there is an underlying cause of a brain injury, it needs to be treated effectively. Age, diabetes, and high blood pressure will all impede full recovery from homonymous hemianopsia.

Homonymous hemianopsia can severely affect what a person is able to see within their visual field. Because of how the brain communicates with the eyes, homonymous hemianopsia can cause a person with an injury to the left side of the brain to lose part of the right visual field in each eye, and vice versa.

If you find yourself bumping into items or having trouble navigating while walking, consider having a visual field acuity test done to diagnose homonymous hemianopsia. Strokes, tumors, and traumatic brain injuries are the leading causes of homonymous hemianopsia. By undertaking the same preventative measures to avoid a stroke, the majority of cases of homonymous hemianopsia can be prevented.

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[WEB SITE] Hemianopia: Types, causes, symptoms, diagnosis, and treatment

hemianopiaHemianopia, also referred to as hemianopsia, comes from a culmination of three different Greek words: “hemi” translates to “half,” “an” translates to “without,” and “opsia” translates to “vision.” Hence, it literally means “being without half of your vision.”

This is a condition where half of your visual field can either be completely blind or partially diminished as a result of head trauma, a tumor, or suffering a stroke.

People who suffer from migraine headaches may sometimes experience temporary hemianopia or other visual disturbances, but this typically subsides on its own after a migraine goes away.

Homonymous hemianopia occurs when you lose part of your visual field on the same side of both eyes. This happens frequently to stroke patients or people who’ve suffered traumatic brain injuries. Visual images that are captured on the left side of the brain are communicated to the right side and vice versa, which is why hemianopia typically affects the same side of each eye equally.

The opposing posterior sides of the brain correspond to the opposite eye, which means that if an injury occurs on the left side of the brain, the visual field defects occur in the right eye.

What are the types of hemianopia?

As an umbrella medical term, there are actually five types of hemianopia and two subcategories in total. In fact, the hemianopia type that a patient suffers from is typically correlated with the exact site of the visual field defect.

Homonymous hemianopia

Visual field is lost on the same side in both eyes, depending on which side of the brain is affected by a stroke or injury. The left optic nerve controls the right visual field and the right optic nerve controls the left visual field. The diminished vision is instrumental in helping doctors locate the exact area of the brain that’s been injured or where the stroke occurred.

Heteronymous hemianopia

Loss of vision occurs in different fields of the eyes. Heteronymous hemianopia is separated into two different categories:

Binasal hemianopia: Blindness or vision loss occurs in the field of vision that’s within the closest proximity to the nose. This is caused by lateral damage to the retinal nerve fibers that don’t cross in the optic chiasm. They’re also responsible for registering information and sending it to the temporal retina.

Bitemporal hemianopia: As the name suggests, bitemporal hemianopia is a loss of vision that happens on the side of the eyes that’s closest to the temple. Lesions and damage to the optic chiasm can cause bitemporal hemianopia. The optic chiasm is located near the pituitary gland where the nerves from the left and right eyeballs meet and cross over one another to reach the opposite side of the brain.


Loss of vision occurs in one quadrant or portion of the visual field, and this usually depends on the part of the brain that’s damaged. The area that’s connected to the damaged portion of the brain will suffer either partial or complete hemianopia.

Superior hemianopia:Superior hemianopia is when loss of vision occurs in the upper visual field of either the left or right eye or both.

Inferior hemianopia:Inferior hemianopia is when loss of vision occurs in the lower visual field of either the left, right, or both eyes.

What causes hemianopia?

There are several different factors or injuries that can cause hemianopia including brain injuries, strokes that occur in certain parts of the brain, and physical head trauma.

As mentioned, while severe migraines can cause temporary hemianopia and adversely affect the patient’s vision, this symptom typically subsides on its own once the migraine pain is relieved.

However, there are more permanent and hazardous causes of permanent hemianopia.

Brain injuries

Damage to certain parts of the brain such as blunt force trauma due to an accident or sports injuries accumulated over an extended period of time can lead to hemianopia in the visual fields of the eyes. These injuries can incur the growth of lesions or contusions on the brain over long periods of time, which can cause hemianopia in old age or even earlier on in life depending on the severity and frequency of the injuries.

Brain tumors

As brain tumors begin to form and continue to grow over time, they can have the same effects as traumatic brain injuries. Eventually, the pressure and damage caused by the tumor can directly result in hemianopia in either one or both of the eyes.


Strokes typically occur as a result of insufficient supply of oxygen reaching the brain. Oxygen is important because it promotes healthy and stable cranial functions. The blockages happen for a number of reasons, the most common one being the formation of blood clots. Depending on the severity of the stroke, it could be fatal for the person who endures it. While survival is certainly preferable, it also means enduring various physical and mental ailments, including hemianopia.

What are the symptoms of hemianopia?

Hemianopia has a variety of signs and symptoms that are associated with it, including the following:

  • Loss of peripheral vision on one or both sides of the face
  • Loss of visual awareness
  • Constantly bumping into people or objects on a regular basis
  • Failing to notice objects or people on the side of the face where the hemianopia damage has occurred
  • Inability to process entire sentences, phrases, or words when reading due to disturbed or interrupted visual patterns
  • Visual hallucinations, as in seeing things that aren’t necessarily there such as certain lighting effects

In addition to the physical indicators of hemianopia, there are also a few psychological, emotional, cognitive, and even social repercussions. Many patients who suffer from hemianopia can become increasingly frustrated or frightened as their condition worsens because it can make mobility and attending social events extremely difficult. As a result, this loss of field vision can also have a negative effect on a person’s ability to live independently and a lot of patients may become gradually reclusive because they fear the outside world and enduring potential injuries.

Mounting irritation, aggravation, and stress also accompany hemianopia because people who suffer from it constantly think that people are bumping into them or objects are appearing out of nowhere. This can make it virtually impossible to function normally in crowded places. Part of the problem is that a lot of people don’t even realize that they have hemianopia until they’re officially diagnosed with it.

How is hemianopia diagnosed?

In order to accurately diagnose hemianopia, your optometrist will most likely send you to a specialist who will then conduct a series of tests on your vision. They’ll start off by asking you a series of questions with the intent of gaining a thorough and clear understanding of the symptoms you’re experiencing. You’ll also undergo a series of visual tests using a machine called a Humphrey Field Analyzer.

This machine tests the depth of vision in each eye individually. It flashes lights in each possible point of your vision including the upper left, lower left, upper right, lower right, and the center. All you have to do is press a button to indicate when you see the light. If the machine detects that you’ve missed the light multiple times in the same areas, it’ll determine that there may be blank patches within your visual field and this is an indication that you may have hemianopia.

Following this assessment, if it’s determined that you do have hemianopia, your doctor may then order a series of MRI tests to establish the initial cause of this condition, whether it was a brain injury, stroke, or a tumor.

How is hemianopia treated?

It’s important to note that while hemianopia treatments can be highly effective and rehabilitative, there’s no actual cure for this condition and you will have to continuously undergo various relief methods that can only stand to improve the condition and make it more manageable.

That said, the following is a list of treatment options for hemianopia. It’s up to your doctor to determine which one would be the most suitable for you depending on the type and severity of the hemianopia you have. In some cases, it might even be appropriate and useful to incorporate a combination of these treatments. Again, your doctor will typically use their own expertise and discretion in such cases.

Visual restoration therapy

This is provided by NovaVision and uses computerized software to help improve patients’ vision in half-hour increments where the patient is instructed to focus their gazes on a specified point and must move their head whenever they see a flash of light or other stimuli in their field of vision. This information is recorded by the computer and the treatment is adjusted with each session and progress of the patient.

Audio-Visual stimulation training

This is a multi-sensory visual training approach to attempting to improve the visual fields of people who suffer from hemianopia and it’s especially effective for treating homonymous hemianopia. It stimulates both the auditory and visual senses in an attempt to get them to work harmoniously with one another and improve the patient’s quality of life despite having this condition.

Optical visual span expanders

These are specialized sunglasses that are formulated specifically for each individual patient and their level of hemianopia. The sunglasses have prisms embedded in their lenses that can help enhance the patient’s vision and expand their field of vision while wearing them.

Explorative saccade training

Also referred to as scanning therapy, this technique tests the speed and correlation with which both eyes move from one focal point to another. The optometrist will observe as the patient’s eyes jet from one vertical or horizontal focal point to another and examine whether the eyes separate or move in unison. People who suffer from hemianopia are taught to incorporate this visual technique in their everyday lives to help them naturally expand their field of vision in every direction.

How does hemianopia effect everyday life?

Hemianopia can have a detrimental effect on a person’s everyday life if left untreated. Especially as people get older, they tend to become more reclusive due to this condition because they feel like burdens to their loved ones and everyone around them. People with diminished eyesight may have a hard time moving around without bumping into people or objects and because their line of vision is diminished as well, they most likely will have to surrender their driving privileges as well. This can make them feel like an even greater burden on their family and friends if they need to be driven everywhere or require the special assistance of a loved one or caregiver.

Hemianopia will undoubtedly have a strong impact on your everyday life, but that doesn’t mean it has to hold you back from being able to resume your regular activities or from doing the things you enjoy. By learning proper management and adaptation techniques, you can learn to live with and even conquer symptoms associated with hemianopia. If you’ve recently suffered a stroke, brain injury, or tumor and are noticing a vast decline in your vision, express these concerns to your doctor immediately so that they can start taking steps to administer a helpful treatment plan.

Related: How to improve vision: 11 home remedies to improve eye health

Related Reading:

Blurred vision in one eye: Causes, symptoms, and home remedies

Ocular migraine (retinal migraine): Causes, symptoms, and treatment



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[WEB SITE] Stroke Victims Look to Innovative Glasses to Improve Side Vision

CORONA, Calif.May 3, 2016 /PRNewswire/ — In addition to being the fourth leading cause of death in the United States, strokes can lead to any number of life-changing disabilities. One of the most common side effects of the estimated 800,000 strokes that occur each year in the country is a loss of side vision (hemianopsia) of up to one-half to the right or the left. With May being both “Stroke Prevention Month,” as well as “Healthy Vision Month,” there is a new focus on the challenges patients with stroke-related hemianopsia face, as well as the hope that advanced Side Vision Awareness Glasses (SVAG) can provide.

Logo –

“When individuals experience hemianopsia much more than just their side vision is reduced,” says Richard Shuldiner, OD, founder of The International Academy of Low Vision Specialists (IALVS), “Their quality of life diminishes, too.”  So concerned about bumping into others or accidentally walking off a curb or into traffic, the condition can leave patients feeling insecure in unfamiliar surroundings. Some avoid going out altogether; others struggle to make it through the day. Though no treatment can actually restore the lost field of vision for these patients, Side Vision Awareness Glasses (SVAG) serve as optical field expansion devices that can increase patients’ viewing fields, improve their safety and enhance confidence.  So effective, patients with custom-made SVAG typically experience an increase of about 15 degrees in side vision awareness immediately upon putting them on. The use of SVAG may even allow some patients to resume driving.

Developed by IALVS member Dr. Errol Rummel, Director of the Neuro-optometric Rehabilitation Clinic at the Bacharach Institute for Rehabilitation in Pomona, NJ, SVAG represents an important advancement over other devices that came before them.  Crafted of lens materials known to minimize distortion, they are noticeably thinner. Also, there is no obvious line in front of the lens, no “thick button,” and no lens strip inserted through the front of the lens. The front of SVAG’s lenses is smooth and barely distinguishable from ordinary glasses.

More important than being better looking than previous devices designed to manage the condition, SVAG provides far-improved vision by offering the widest viewing area. Their vertical edge enables a person with hemianopsia to move their eyes just a few millimeters to access the SVAG area of the lens. Unlike devices that superimpose a narrow peripheral image over a person’s central vision, SVAG is easier for patients to use, as well as to learn to use. They’re also harder to break, because there is no glued seam splitting through the lens from front to back.

Patients with hemianopsia who are acutely aware of their side vision loss can often be trained to scan their eyes to compensate for their impairment, but for those who are unaware or inattentive to the condition, which doctors term “hemianopsia with neglect,” SVAG can go beyond increasing their field of vision—they can broaden their worlds.

In any case, a qualified low vision optometrist can help you determine whether Side Vision Awareness Glasses are right for you or a loved one.  All members of The International Academy of Low Vision Specialists are low vision optometrists with extensive training and experience in assisting patients suffering from stroke-related hemianopsia. To locate a member near you, simply visit their website: or call 1-888-778-2030.

For more information, contact:

Tracy LeRoux, The Link Agency, Inc.

(800) 291-0530


SOURCE International Academy of Low Vision Specialists

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[ARTICLE] Segregation of Spontaneous and Training Induced Recovery from Visual Field Defects in Subacute Stroke Patients – Full Text

Whether rehabilitation after stroke profits from an early start is difficult to establish as the contributions of spontaneous recovery and treatment are difficult to tease apart. Here, we use a novel training design to dissociate these components for visual rehabilitation of subacute stroke patients with visual field defects such as hemianopia. Visual discrimination training was started within 6 weeks after stroke in 17 patients. Spontaneous and training-induced recoveries were distinguished by training one-half of the defect for 8 weeks, while monitoring spontaneous recovery in the other (control) half of the defect. Next, trained and control regions were swapped, and training continued for another 8 weeks. The same paradigm was also applied to seven chronic patients for whom spontaneous recovery can be excluded and changes in the control half of the defect point to a spillover effect of training. In both groups, field stability was assessed during a no-intervention period. Defect reduction was significantly greater in the trained part of the defect than in the simultaneously untrained part of the defect irrespective of training onset (p = 0.001). In subacute patients, training contributed about twice as much to their defect reduction as the spontaneous recovery. Goal Attainment Scores were significantly and positively correlated with the total defect reduction (p = 0.01), percentage increase reading speed was significantly and positively correlated with the defect reduction induced by training (epoch 1: p = 0.0044; epoch 2: p = 0.023). Visual training adds significantly to the spontaneous recovery of visual field defects, both during training in the early and the chronic stroke phase. However, field recovery as a result of training in this subacute phase was as large as in the chronic phase. This suggests that patients benefited primarily of early onset training by gaining access to a larger visual field sooner.


Loss of up to one-half of the visual field (hemianopia) as result of post-chiasmatic stroke in one hemisphere occurs in about 30% of all stroke patients. Following a period of spontaneous recovery in the first 3–6 months (12), the patient enters the chronic phase of hemianopia.

Rehabilitation treatment most often involves eye movement training to compensate for the visual field defect (3) rather than visual restitution training, which reduces the defect itself. The latter has long been controversial (4). However, a recent series of investigations (512) have argued for the more balanced view that visual training of the defect may provide an additional and valuable approach to rehabilitation of occipital stroke patients.

Brain plasticity is believed to be greater in the acute stage after stroke when there is a window for relatively quick and extensive synaptic reorganization (13). Recommendations that rehabilitation should begin “as soon as possible” or “early” are therefore common in clinical guidelines (1415). However, many of these recommendations are based on limited data (16), and there are no agreed definitions of what constitutes early rehabilitation (17). Thus far, visual restitution training is generally applied in the chronic phase after stroke, so that spontaneous recovery can be excluded, and changes in the visual field can be attributed to training. In this way, one can obtain an accurate estimate of the effect of the training itself (811). Yet, we wondered if visual restitution training would profit from an early start as suggested in the rehabilitation literature.

The effect of visual perceptual learning in normally sighted subjects is often restricted to the trained region of the visual field (1820) and specific to the trained task (2122). This raises the question whether the visual recovery that is induced by visual restitution training is also limited to just the trained region and task. Several studies have shown that recovered vision after restitution training transfers to untrained visual tasks (1011) but only to a limited extent to untrained regions. For example, the defect reduction induced by training of the intact visual hemifield was significantly smaller than the reduction induced by training the affected hemifield itself, and it was not significantly different from the defect reduction following a non-intervention period (11). Because spontaneous recovery could be excluded in that study, any improvement during intact training could point to a spillover effect of training between the two hemispheres. That is, the defect reduces—albeit to limited extent—even when another part of the visual field is trained.

Following the practice of general rehabilitation medicine, one would preferably train patients in the early phase of stroke. To do so, we applied a method that builds on the observation that visual training carries over to neighboring areas only to a limited extent. That is, we used two training rounds, which targeted complementary parts of the defect [regions of interest (ROIs)], while monitoring in both training rounds the trained and the untrained half of the defect. The untrained half of the defect, which serves as an internal control for the trained half, will show spontaneous recovery and a potential spillover from the neighboring trained region. To assess that spill over, we used data from seven patients who were trained in the chronic phase of stroke using the same method. The differences between the defect reductions for the subacute phase of stroke and the chronic phase of stroke in the trained and untrained parts of the defect should allow us to distinguish between spillover, spontaneous recovery and training-induced recovery. This allows us to test the hypothesis that training in the early phase leads to a larger defect reduction than training in the chronic phase.

Materials and Methods

The study was approved by the ethical committee CMO Arnhem–Nijmegen in correspondence with the 1964 Declaration of Helsinki.

20 Subacute stroke patients and 10 chronic stroke patients with visual field defects due to post-geniculate damage were included following written informed consent. Subacute stroke patients were screened for participation in four neurology departments of Dutch hospitals: UMC in Utrecht, St. Elisabeth Hospital in Tilburg, CWZ in Nijmegen and St. Antonius Hospital in Nieuwegein (screening; eight patients). Patients could also sign up for the study by filling out a form on our website (; 12 patients), to be screened at a regional office by the first author. Chronic stroke patients all applied through the website.

Patients inclusion criteria as follows:

∗ age between 18 and 75 years;

∗ presence of homonymous visual field defect.

Patient exclusion criteria as follows:

∗ visual neglect (as assessed by line bisection test);

∗ cardiac or other implants (for the chronic patients only: MRI scans were made; to be presented elsewhere).

The intake procedure included a Goldmann perimetry measurement. Patient demographics can be found in Table S2 in Supplementary Material.

For the 30 included patients, we had to exclude the data of 3 subacute and 3 chronic patients from further analysis. In the three subacute patients, the training was not applied as intended because the defect was not divided in two equal halves (n = 2), or for unequal duration of the training rounds (n = 1). In the chronic patients, absence of an absolute defect (n = 1), inability to cope with training demands (n = 1), and anxiety for fMRI scanner measurements (n = 1) were reasons to exclude their data. Thus, in total, we analyzed 17 subacute and 7 chronic data sets.

The 20 subacute patients were trained by DB for this study, the 10 chronic patients were trained by JE in a parallel study using the same training paradigm.

Study Design

Before the training, baseline values were established for visual field size (Goldmann perimetry), reading speed and Goal Attainment Scaling (GAS: personally customized and realistic goals).

Following these baseline measurements, the visual field defect was divided in equal halves using the following procedure. First, meridional angles through the defect were established that were farthest apart. Then, the average of these two outer meridional angles formed the border between the two training regions (in the case of SA15, the division was along the vertical midline). One-half of the visual field defect was trained for 8 weeks, while the other half was untrained. After this period, intermediate measurements were carried out (perimetry and reading speed tests) during the course of one week. Then, a second training period of 8 weeks was started, in which the training was applied to the other half of the defect, while the first half received no further training. Post-measurements were carried out as during baseline measurements (Figure 1). Finally, we collected follow-up perimetry data in the subacute group. The period without training, in-between the final training session and the follow-up perimetry of the subacute group, is denominated “No Intervention.”

Figure 1. Study design and time line for subacute patients. The defect was divided into two training regions [region of interest (ROI) 1, ROI 2] of equal size. In this example, the left upper quarter field was trained first, followed by the lower left quadrant. This order was randomized between patients. For chronic patients, the study design was similar, except that the first training started at least 10 months after the stroke (and about 2 months after intake), and no follow-up measurements were taken.

Continue —>  Frontiers | Segregation of Spontaneous and Training Induced Recovery from Visual Field Defects in Subacute Stroke Patients | Neurology

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[ARTICLE] Audiovisual Rehabilitation in Hemianopia: A Model-Based Theoretical Investigation – Full Text

Hemianopic patients exhibit visual detection improvement in the blind field when audiovisual stimuli are given in spatiotemporally coincidence. Beyond this “online” multisensory improvement, there is evidence of long-lasting, “offline” effects induced by audiovisual training: patients show improved visual detection and orientation after they were trained to detect and saccade toward visual targets given in spatiotemporal proximity with auditory stimuli. These effects are ascribed to the Superior Colliculus (SC), which is spared in these patients and plays a pivotal role in audiovisual integration and oculomotor behavior. Recently, we developed a neural network model of audiovisual cortico-collicular loops, including interconnected areas representing the retina, striate and extrastriate visual cortices, auditory cortex, and SC. The network simulated unilateral V1 lesion with possible spared tissue and reproduced “online” effects. Here, we extend the previous network to shed light on circuits, plastic mechanisms, and synaptic reorganization that can mediate the training effects and functionally implement visual rehabilitation. The network is enriched by the oculomotor SC-brainstem route, and Hebbian mechanisms of synaptic plasticity, and is used to test different training paradigms (audiovisual/visual stimulation in eye-movements/fixed-eyes condition) on simulated patients. Results predict different training effects and associate them to synaptic changes in specific circuits. Thanks to the SC multisensory enhancement, the audiovisual training is able to effectively strengthen the retina-SC route, which in turn can foster reinforcement of the SC-brainstem route (this occurs only in eye-movements condition) and reinforcement of the SC-extrastriate route (this occurs in presence of survived V1 tissue, regardless of eye condition). The retina-SC-brainstem circuit may mediate compensatory effects: the model assumes that reinforcement of this circuit can translate visual stimuli into short-latency saccades, possibly moving the stimuli into visual detection regions. The retina-SC-extrastriate circuit is related to restitutive effects: visual stimuli can directly elicit visual detection with no need for eye movements. Model predictions and assumptions are critically discussed in view of existing behavioral and neurophysiological data, forecasting that other oculomotor compensatory mechanisms, beyond short-latency saccades, are likely involved, and stimulating future experimental and theoretical investigations.


The primary human visual pathway conveys the majority of retinal fibers to the lateral geniculate nucleus of the thalamus and then, via the optic radiations, to the primary visual cortex (V1) (the retino-geniculo-striate pathway). V1 is the main distributor of visual information to extrastriate visual areas, for further processing. A secondary visual pathway (the retino-collicular pathway) routes a minority of retinal fibers directly to the Superior Colliculus (a midbrain structure), which also has reciprocal connections with striate and extrastriate visual cortices (May, 2006).

Patients with lateralized damages to the primary visual cortex (V1) or to the neural pathway feeding V1 often develop homonymous hemianopia, a visual field defect with the loss of conscious vision in one hemifield. Hemianopic patients cannot perceive visual stimuli presented in the blind hemifield; moreover, they show the inability to spontaneously develop effective oculomotor strategies to compensate for the visual field loss (Hildebrandt et al., 1999Zihl, 2000Tant et al., 2002).

Despite the visual deficit, hemianopic patients can preserve the ability to integrate audiovisual stimuli in the affected field, with beneficial effects (Frassinetti et al., 2005Leo et al., 2008). In particular, data by Frassinetti and colleagues (Frassinetti et al., 2005) show that patients performing a visual detection task, while maintaining central fixation, significantly improved conscious visual detections in the affected field, when the auditory stimuli were applied in spatial and temporal coincidence with the visual targets.

The Superior Colliculus is the most likely structure mediating this multisensory improvement, because of its anatomical connections and the properties of its neuronal responses. Indeed, SC neurons receive not only visual information but also signals from other different sensory modalities, such as audition (Meredith and Stein, 1986Stein and Meredith, 1993May, 2006). Visual and auditory information are integrated in multisensory SC neurons according to specific principles (Stein and Meredith, 1993): an audiovisual stimulation elicits a stronger neuronal activation than each single component, when the visual and auditory components are presented in spatial and temporal register (spatial and temporal principle). Moreover, a proportionally greater enhancement of multisensory neuronal activation is evoked when weakly effective unisensory stimuli are combined, compared to the combination of highly effective stimuli (inverse effectiveness principle). The SC integrative principles have strong implications in hemianopia, as the SC and the retino-collicular pathway are preserved in these patients. Visual retinal input to SC, although weak, can still be efficiently combined with an accessory auditory input thanks to the inverse effectiveness principle, provided the rule of spatial and temporal proximity is satisfied. Furthermore, SC multisensory enhancement can affect cortical visual processing thanks to the projections from the SC to the visual cortices.

In addition to the immediate, “online” multisensory improvement in visual detection, there is also evidence of prolonged, “offline” effects that can be induced by repeated exposure to audiovisual stimuli. Indeed, long-lasting improvements of visual performances in hemianopic patients, promoted by audiovisual training protocols stimulating the blind hemifield, have been reported (Bolognini et al., 2005Passamonti et al., 2009Dundon et al., 2015bTinelli et al., 2015Grasso et al., 2016). During the training, a visual target was given in close spatial and temporal proximity with an auditory stimulus, at various positions in the visual field; patients were asked to detect the presence of the visual target, by directing the gaze toward it from a central fixation point. Results revealed a significant post-training improvement in detection of unimodal visual targets in the blind field when the patients were allowed to use eye movements, while a weak amelioration was found when they had to maintain central fixation (Bolognini et al., 2005Tinelli et al., 2015). Such results suggest that the audiovisual training could promote an increased oculomotor response to visual stimuli in the affected hemifield.

Beyond the “online” effects of audiovisual stimulation, the Superior Colliculus is a possible candidate for mediating the training effects, too. Indeed, the SC projects to brainstem motor areas controlling eyes and head orientation, and is critically involved in the initiation and execution of reflexive (i.e., exogenously-driven) saccades (Sparks, 1986Jay and Sparks, 1987aMay, 2006Johnston and Everling, 2008). Importantly, more than 70% of SC neurons projecting to the brainstem and, therefore involved in saccade generation, respond to multisensory stimulations (Meredith and Stein, 1986). As such, audiovisual stimuli, enhancing multisensory SC activation, might plastically reinforce the gain of the transduction from the SC sensory response to the motor output; in other words, after training the oculomotor system could have acquired increased responsiveness to the visual input conveyed via the retino-collicular pathway. However, the plastic mechanisms and synaptic reorganization that can functionally instantiate these visuomotor capabilities remain undetermined. Moreover, it is unclear whether the training may even stimulate genuine visual restitution beyond oculomotor compensation, and how the compensatory and restitutive effects may complementary contribute to visual improvements.

Recently, we have developed a neural network model (Magosso et al., 2016) that formalized the main cortico-collicular loops involved in audiovisual integration, and implemented—via neural connections and input-output neural characteristics—the SC multisensory integrative principles. The network postulated neural correlates of visual consciousness and mimicked unilateral V1 lesion. Simulations, performed in fixed-eyes condition, reproduced the “online” effects of enhanced visual detection under audiovisual stimulation.

Here, we extend our previous neural network to explore the effects of training in simulated hemianopic patients, providing quantitative predictions that can contribute to a mechanistic understanding of visual performance improvement observed in real patients. To this aim, the network has been integrated by novel elements. First, we have included a module of saccade generation, embracing the colliculus sensory-motor transduction; in this way, we can account for the potentiality of short-latency saccades triggered in a bottom-up fashion. Second, Hebbian mechanisms of synaptic learning have been implemented and adopted during training simulations. Different training paradigms (audiovisual multisensory/visual unisensory stimulation in eye-movements/fixed-eyes condition) are tested, to examine their efficacy in promoting different forms of rehabilitation (compensatory/restitutive), and to assess the predicted results in light of in vivo data.


Materials and Methods

The neural network is conceptually made up of two modules (Figure 1A). A sensory module (blue blocks and lines) includes cortical and subcortical (SC) neuronal areas devoted to the sensory representation of the external stimulation. An oculomotor module (red blocks and lines) can potentially react to the sensory neural representation, generating a saccade toward the external stimulation. The SC is involved in both modules.

Figure 1. (A) Sketch of the neural network architecture. Blue blocks and lines represent the sensory module; red blocks and lines denote the oculomotor module. R, retina; V1, primary visual cortex; E, extrastriate visual cortex; SC, Superior Colliculus; A, auditory area; FP, saccade-related frontoparietal areas (δ denotes a pure delay); SG, Brainstem Saccade Generator. g(t) is the current gaze position (resulting from the oculomotor module); θg is the target gaze position decoded from the SC activity. pis the position of the external (visual or spatially coincident audiovisual) stimulus in head-centered coordinates, and p-g(t) is the stimulus position in retinotopic coordinates. WH, Q denotes inter-area synapses from neurons in area Q to neurons in area H(B) Exemplary pattern of basal (i.e., pre-training) inter-area synapses. Here, synapses WSC, R from the retina to SC are depicted, limited to about one hemifield (−10° ÷ +90°) (the same pattern holds for the remaining not shown positions). x-axis reports the position (j, in deg) of the pre-synaptic neuron in area R and the y-axis the position (i, in deg) of the post-synaptic neuron in area SC. The color at each intersection (j, i) codes the strength of the synapse from the pre-synaptic neuron j in area R to the post-synaptic neuron i in SC. Similar patterns hold for all other inter-area synapses within the sensory module. Consistently with the following figures, scale color is between 0 and the maximum value reachable by training (WSC,RmaxWmaxSC,R). WSC,R0W0SC,R denotes the central weight of the pre-training Gaussian pattern of the synapses. (C) Schematic picture of the eye-centered topological organization of neurons in each area. In case (1), the stimulus induces an activation bubble centered on the neuron with preferred retinal position = 45°, in a given area; in case (2), the stimulus induces an activation bubble centered on the neuron with preferred retinal position = 45°–30° = 15°.

Continue —> Frontiers | Audiovisual Rehabilitation in Hemianopia: A Model-Based Theoretical Investigation | Frontiers in Computational Neuroscience

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[VIDEO] How to Biology & Anatomy: Optic pathways, visual fields and the lesions – YouTube


See the original video here: Created by Dale Ledford, a college Biology, Human Anatomy, and Physiology instructor in Blountville, Tennessee.

via How to Biology & Anatomy: Optic pathways, visual fields and the lesions – YouTube

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[VIDEO] Homonymous Hemianopia – YouTube

via Homonymous Hemianopia – YouTube

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