To provide a systematic overview of interventions for stroke related visual impairments.
Background: Ischemic stroke are lack of blood flow to the brain and it could influence the visual field. Approximately more than half of the ischemic stroke patient have visual defect.
Objective : Disturbance of blood flow on visual pathway have impact to the visual field defect. In stroke ischemic patient, recirculation of penumbra at the brain on the third months after onset can rehabilitate the visual pathway, also it will improve the outcome of visual filed defect. So it could be initial detection for rehabiltation of visual field defect.
Methods: This study was intended to compere visual field defect of ischemic stroke patient after three months therapy conducted form September 2014 – February 2015 in Mohammad Hoesin General Hospital Palembang. A total of 12 patients who met the inclusion criteria were recruited by consecutive sampling. All patients were endure based on ophthalmology and visual field examination using Humphrey Field Analyzer twice. First after relieving from the attack of stroke and second after three months therapy. Measurement of standard have to compare the value of MD, VFI, PSD, PD and pattern visual field defect.
Results: There were significant difference in value of MD, VFI, PSD and PD<0,5% for both eyes on stroke ischemic patients after three months therapy. Almost all variable value were increasing to improvement of defect. The most common type of visual field defect is homonymous hemianopia.
Conclusion: There were improvement in visual field defect in patients with stroke ischemic after three months therapy.
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In this article, the authors focus on rehabilitation of patients with acquired brain injury from both traumatic and nontraumatic causes. Rehabilitative strategies include both restorative therapies that serve to regain function and compensatory strategies that allow for compensation of lost function. Rehabilitation can occur in both inpatient and outpatient settings and involves multiple providers, including physical therapists, occupational therapists, and speechlanguage pathologists. This review will focus on the functional impairments that arise from acquired brain injury and the role of rehabilitative strategies to enhance neurologic recovery and improved functional outcomes.
Partial and homonymous visual field loss (HVFL) is a common consequence of post-chiasmatic injury to the primary visual pathway or injury to the primary visual cortex. Different approaches to rehabilitation have been reported for older adults with HVFL and there is evidence to support the use of compensatory training over other proposed therapies. We reviewed the literature to investigate the current state of the art of rehabilitation and habilitation strategies for children and young people with HVFL, and whether there is enough evidence to support the use of these strategies in the paediatric population. We have provided an overview of the existing literature on children and young people with HVFL, a brief overview of rehabilitation strategies for adults with HVFL, and evidence on whether these different interventions have been applied with children and young people effectively. We found that there have been very few studies to investigate these strategies with children and young people, and the quality of evidence is currently low. New research is required to evaluate which strategies are effective for children and young people with HVFL and whether new strategies need to be developed.
Hemianopia explained and simulated using an eye-tracker
Strategies for adapting a computer for use by people with visual field deficits.
Hemianopia leads to severe impairment of spatial orientation and mobility. In cases without macular sparing an additional reading disorder occurs. Persistent visual deficits require rehabilitation. The goal is to compensate for the deficits to regain independence and to maintain the patient’s quality of life. Spontaneous adaptive mechanisms, such as shifting the field defect towards the hemianopic side by eye movements or eccentric fixation, are beneficial, but often insufficient. They can be enhanced by training, e.g., saccadic training to utilize the full field of gaze in order to improve mobility and by special training methods to improve reading performance. At present only compensatory interventions are evidence-based.
This is part one of a three-part article published to health.mil.
Vision Problems After Brain Injury
Visual problems following brain trauma are frequent and often complex. It is probably easiest to define the problems based upon how they affect incoming visual information (i.e., the afferent visual pathways) or the outflow of information to the visual organs (i.e., efferent visual pathways). Afferent defects include reduction in visual acuity, visual field, color vision, contrast sensitivity, comfort (usually as it relates to glare), and higher level visual processing, including recording of visual memory and comprehension of visual stimuli. Efferent defects include reduction of the ability to visually pursue a target, focus the lens inside the eye, train the two eyes onto a single target, maintain gaze once a visual target is obtained, and open and close the eyelids. In this three part series, we will describe 1) damage to the afferent visual pathways, 2) damage to the efferent visual pathways, and 3) the role of the neuro-ophthalmologist in visual restoration and rehabilitation.
The Afferent Visual Pathway and How Brain Injury Can Affect It
Light enters the eye through the cornea, the clear window of the eye. The cornea provides the majority of the focusing power of the eye, and is an extremely poor refractive surface, but with a healthy tear film it becomes nearly perfect. Brain injury often causes dry eye thereby reducing visual acuity. Furthermore, brain injury patients often lose an adequate blink response or develop lagophthalmos, the inability to completely close the eye. Dry, unprotected corneas are subject to scarring and infection.
Trauma to the brain often entails injury that can also shake or directly damage the eye along with the rest of the body. Patients suffering a blast injury can experience rapid elevation of pressure in the chest, which is then transmitted by the blood vessels to the retina, the neural tissue lining the inner wall of the eye. This is the tissue which converts light rays into the electrical impulses that are sent to the brain. The retinal blood vessels can rupture from the sudden increase in pressure and cause bleeding within the retina, a condition called Purtscher’s retinopathy. The free blood inside the eye can cause significant scarring and loss of vision.
Direct head trauma can also cause the eye to move too quickly and/or too far relative to the fixed structures in the eye socket. This can cause stretching or shearing of the optic nerve, the nerve that carries visual information to the brain. This traumatic optic neuropathy often can result in permanent visual impairment. Multiple direct head traumas also are a risk factor for problems within the eye itself, such as detachment of the retina from the back of the eye, or formation of a cataract, a clouding of the natural lens.
Trauma to the head invariably is associated with some degree of trauma to the neck, a risk factor for damage to the blood vessels of the neck. Injury to the wall of an artery can cause it to bulge (i.e., form an aneurysm) or separate from its inner lining (i.e., arterial dissection). Either situation can lead to abnormal blood flow to the visual pathways of the brain. Furthermore, either condition can cause the vessels to physically compress portions of the visual pathways, such as the nerves that control the eye muscles or the nerves that bring visual information to the brain. This could result in double vision or in reduction of visual acuity and visual field, respectively.
It has been demonstrated that the world we see is formed into a map upon our brain, specifically onto an area called the visual cortex. This map is organized such that the image of the world is inverted and reversed; the left side of our brain sees what is to the right of where we look and the right side of the brain sees light from the left of where we gaze. Furthermore, visual information emanating from above our visual point of interest is transmitted to the lower portion of the visual cortex while the upper portion of the visual cortex maps the visual world below the object of regard. It is for this reason that damage to the visual cortex causes loss of peripheral vision rather than simply loss of visual clarity.
While we do not know how visual memories are created or stored in our brains, it is known that brain injury slows the acquisition and processing of visual information and impairs the formation of visual memory. Recent research has suggested that these impairments may result from stretching or shearing of nerve fiber bundles after head injury. Sadly, higher level visual processing failure is often particularly difficult for a patient to express. Neuropsychologists have proven to be critically important for the diagnosis of these problems and for guidance in directing rehabilitation efforts.
From Stars and Stripes, March 2010, Health.mil.
To provide a systematic overview of interventions for stroke related visual impairments.
A systematic review of the literature was conducted including randomized controlled trials, controlled trials, cohort studies, observational studies, systematic reviews, and retrospective medical note reviews. All languages were included and translation obtained. This review covers adult participants (aged 18 years or over) diagnosed with a visual impairment as a direct cause of a stroke. Studies which included mixed populations were included if over 50% of the participants had a diagnosis of stroke and were discussed separately. We searched scholarly online resources and hand searched articles and registers of published, unpublished, and ongoing trials. Search terms included a variety of MESH terms and alternatives in relation to stroke and visual conditions. Article selection was performed by two authors independently. Data were extracted by one author and verified by a second. The quality of the evidence and risk of bias was assessed using appropriate tools dependant on the type of article.
Forty-nine articles (4142 subjects) were included in the review, including an overview of four Cochrane systematic reviews. Interventions appraised included those for visual field loss, ocular motility deficits, reduced central vision, and visual perceptual deficits.
Further high quality randomized controlled trials are required to determine the effectiveness of interventions for treating post-stroke visual impairments. For interventions which are used in practice but do not yet have an evidence base in the literature, it is imperative that these treatments be addressed and evaluated in future studies.
Visual impairments following stroke may include abnormalities of central and/or peripheral vision, eye movements and a variety of visual perception problems such as inattention and agnosia. The visual problems (types of visual impairment) can be complex including ocular as well as cortical damage (Jones & Shinton, 2006; Rowe et al., 2009a). Visual impairments can have wide reaching implications on daily living, independence, and quality of life. Links with depression have also been documented in the literature (Granger, Cotter, Hamilton, & Fiedler, 1993; Nelles et al., 2001; Ramrattan et al., 2001; Tsai et al., 2003; West et al., 2002). The estimation of the overall prevalence of visual impairment is approximately 60% at the acute stage following stroke (Ali et al., 2013; Barrett et al., 2007; Clisby, 1995; Freeman & Rudge, 1987; Isaeff, Wallar, & Duncan, 1974; Rowe et al., 2009b; Rowe et al., 2013). A review of the individual prevalence figures and the recovery rates for each of the possible post-stroke visual impairments has been reported elsewhere in the literature (Hepworth et al., 2016).
In order to treat and manage visual impairments caused by stroke it is important to establish the range and effectiveness of the available treatment options. The aim of this literature review is to provide a comprehensive synthesis of the evidence relating to treatment of visual problems after stroke.
Patients with peripheral field loss complain of colliding with other pedestrians in open-space environments such as shopping malls. Field expansion devices (e.g., prisms) can create artificial peripheral islands of vision. We investigated the visual angle at which these islands can be most effective for avoiding pedestrian collisions, by modeling the collision risk density as a function of bearing angle of pedestrians relative to the patient. Pedestrians at all possible locations were assumed to be moving in all directions with equal probability within a reasonable range of walking speeds. The risk density was found to be highly anisotropic. It peaked at ’458 eccentricity. Increasing pedestrian speed range shifted the risk to higher eccentricities. The risk density is independent of time to collision. The model results were compared to the binocular residual peripheral island locations of 42 patients with forms of retinitis pigmentosa. The natural residual island prevalence also peaked nasally at about 458 but temporally at about 758. This asymmetry resulted in a complementary coverage of the binocular field of view. Natural residual binocular island eccentricities seem well matched to the collision-risk density function, optimizing detection of other walking pedestrians (nasally) and of faster hazards (temporally). Field expansion prism devices will be most effective if they can create artificial peripheral islands at about 458 eccentricities. The collision risk and residual island findings raise interesting questions about normal visual development.