Visual Field Impairment Research Articles

Clinical provision of compensatory visual training after neurological injury: example of a multisite outpatient program

Aim Treatment efficacy is established via controlled research trials, but treatment in real-world clinical environments is typically highly variable and may differ from research protocols by necessity. Here, we examined provision of visual retraining for adults after neurological injury at an outpatient rehabilitation program in Calgary, Canada. Methods Retrospective chart audits extracted demographic data, assessment outcomes, and details related to provision of training. Results Treatment was provided to individuals with both visual field and visual-perceptual impairments due to neurological injury (mostly stroke). Tools and techniques of visual retraining at this program are discussed, the common denominator being repetitive practice of compensatory visual behaviors. Across this multisite program, there was significant variability in the number of treatment sessions, 13.00 (±10.21) sessions for those with visual-perceptual impairments and 14.41 (±9.63) sessions for those with field loss. Descriptive statistics and confidence intervals suggest improved outcomes on some measures for those with visual field and visual perceptual impairments. Conclusions Our data suggest that visual retraining is feasible in this clinical outpatient setting. Implications for rehabilitation This program of visual retraining was provided to individuals with visual impairment (e.g., hemianopia) and visual perceptual impairment (e.g., unilateral spatial neglect) as a result of neurological injury. In this outpatient program, visual rehabilitation was feasible and appeared to improve outcomes among a heterogeneous clinical population. Fundamental characteristics of visual compensatory training at this program included repetitive practice of adaptive scanning behaviors across multiple contexts to promote automaticity and generalization of skills.

Adjuvant Radiation Therapy Compared with Observation Alone for Postoperative Residual Nonfunctional Pituitary Adenomas

The management of residual nonfunctional pituitary tumors after surgical resection remains controversial. In this study, we compared the prognosis of postoperative radiation therapy and observation only in patients with residual nonfunctional pituitary adenoma and reviewed the long-term complications after radiation therapy. We retrospectively analyzed 90 patients who underwent surgery for nonfunctional pituitary adenomas from January 2008 to April 2012. Residual tumors were classified by size, location, and pathologic staining. Tumor progression was defined as volume progression ≥15% with or without clinical symptoms. Postoperative radiation therapy was performed <1 year after the last surgery. We compared the progression and 3-year and 5-year progression-free survival between the observation group and postoperative radiation therapy group. Postradiation complications including hypopituitarism, diabetes insipidus, deterioration in visual field or acuity, cranial nerve palsy, and hydrocephalus were also analyzed. More of the patients who received postoperative radiation therapy had a tumor progression-free survival of ≥3 years than did those who did not receive postoperative radiation therapy. Postoperative radiation therapy was significantly beneficial for the patients with a tumor size ≥3 cm or with tumors in the cavernous sinus. The most frequent complication after radiation therapy was hypopituitarism and a few cases had third cranial nerve palsy; however, there were no significant relationships with radiation therapy. In this study, immediate radiation therapy after tumor resection was an effective and relatively safe treatment for residual or progressive nonfunctional pituitary adenomas. Moreover, the long-term complications of radiation therapy were mild.

Endoscopic Optic Nerve Decompression: Indications, Technique, Results

For decades, treatment of compressive optic nerve neuropathy was conservative and involved the intravenous application of high-dose corticoids, which was combined with nerve growth factors in later years. If surgery was considered, transcranial and transfacial access to the orbital apex and the optic nerve were achieved using classical approaches. Over the past decade, endonasal endoscopic procedures have increasingly come into force, based on favorable experiences with functional endoscopic sinus surgery and as a result of innovative developments in endoscopy and image guidance. The purpose of this review is to address the latest literature in this field with regard to the indications, techniques, results, and complications associated with this procedure. There are basically two approaches for endoscopic optic nerve decompression: the extradural supraorbital “keyhole” approach, which provides access to the optic nerve canal roof and which is usually performed by neurosurgeons, and the endonasal endoscopic approach, which is widely used by otorhinolaryngologists. The development and application of endonasal endoscopic surgery was only possible with extensive knowledge of the topographic anatomy. The most important anatomical landmarks and topography have been described based on either cadaveric or CT scan studies, and include the opticocarotid recess, the distance between the optic nerve canal and the internal carotid artery, the ophthalmic artery, and the length of the optic nerve canal. There are two main indications for endonasal endoscopic optic nerve decompression: (1) traumatic optic nerve neuropathy (TON), and (2) optic nerve neuropathy from non-traumatic causes (nTON), such as tumorous conditions, inflammatory diseases, or idiopathic intracranial hypertension (IIH). In trauma cases, rates of postoperative visual improvement of 40–80% have been reported. Factors influencing the outcome include the severity of the injury, initial visual acuity (light perception or better vs. no light perception), the time interval between trauma and intervention, and the type of injury, such as fracture lines directly through the optic nerve canal or probable avulsion trauma. nTON cases generally have a slightly better prognosis, with vision improvement of 54–100% reported. The procedure should be performed before any optic nerve atrophy can occur. In IIH cases, all major symptoms, including vision loss, headache, visual field deterioration, and papilla edema, improved after optic nerve decompression, with rates of 60–100% reported. Earlier studies reported the occurrence of major complications such as cerebral fluid leakage, severe hemorrhage, or optic nerve injury at rates of about 3%. However, more recent studies postulate that no major complications occur, which may reflect the increasing use of the endonasal endoscopic route to the optic nerve and skull base as standard procedure, so that surgeons are becoming more comfortable with the technique. Endonasal endoscopic optic nerve decompression is a safe and highly effective treatment to reduce hydrostatic pressure on the optic nerve in cases of optic nerve neuropathy of various etiologies. In TON cases, about 50% of patients will benefit from the procedure, with vision improvement possible in some cases even with an interval of some days between trauma and surgery. Non-trauma cases have a slightly better prognosis. The intervention should be performed prior to optic nerve atrophy.

SUN-448 Giant Prolactinomas: A Follow-Up of 25 Years with Dopamine Agonists

Giant prolactinomas are tumors with a large size > 4 cm and/or prolactin levels higher than 3000 ng/ml and/or highly invasive growth. Today dopamine agonists, mainly cabergoline (CAB), are the first-line choice in the treatment of these tumors. Objective: To assess the efficacy, safety and long-term follow-up of patients with giant prolactinomas treated with dopamine agonists. Methods: We retrospectively reviewed the clinical records of 20 patients with giant prolactinomas. Mean age at diagnosis was: 45.2 ± 18.9 years, 75% men. The median follow-up time was 9.05 years (1.5-25.1). At diagnosis the median prolactin level was 6,545 ng/ml (3,238-15,325), the mean maximum diameter of the tumors was 4.60 ± 1.35 cm. At diagnosis, headaches were present in 55% and hypogonadism in 85% of patients; 80% had invasive tumors and 75% had visual field (VF) impairment. Since the diagnosis, almost all patients were treated with CAB except 2, one with bromocriptine LAR and the other one with oral bromocriptine, both were switched to CAB afterwards. Results: Seventy percent of patients normalized prolactin levels, this was achieved in a median time of 7.5 months (2-26) and with a mean dose 2.14 ±1.19 mg/week of CAB. Fifty-four percent of patients reached this prolactin nadir in 2-4 months with a maximum dose < 2 mg/week. The median prolactin level in the last visit was 31.23 ng/ml (12-147). Ninety percent of patients decreased prolactin level during follow-up: 50% normalized prolactin, 25% remained with a mild hyperprolactinemia, 25% with significant hyperprolactinemia. Ninety-five percent of tumors reduced their volume, 60% evolved to empty sella, the remaining achieved a mean decrease of 3.75 cm compared to the initial size (82% of average reduction compared to the initial diameter). The VF remained normal in patients in whom it was not affected, except in 1 whose VF deteriorated because of chiasmatic ptosis; in the patients who presented VF involvement: 47% improved, 40% remained unchanged and 13% worsened. The complications during the follow-up were: Cerebrospinal fluid leak in 2 patients, chiasmatic ptosis in 1 with VF impairment, intra-tumoral hemorrhage in 1. In the follow-up only 1 patient required surgery; 4 patients died, 2 because of the tumor. In 3 (15%) patients CAB was stopped at 96-180-264 months after treatment was initiated, but in all of them CAB was reinitiated due to symptomatic hyperprolactinemia. In 16 patients the treatment could never be discontinued. Conclusions: CAB was effective in the treatment of giant prolactinomas reducing tumor size (some of them evolved to empty sella) and prolactin levels in most patients, with low-moderate doses of CAB and very few complications. In our experience of 25 years of follow-up, we have not had any patients without treatment.

Glaucoma as a dangerous interplay between ocular fluid and cerebrospinal fluid

Glaucoma is a leading cause of irreversible blindness worldwide. Primary open-angle glaucoma, the most common type, is characterized by progressive degeneration of retinal ganglion cells and their axons in the optic nerve, resulting in progressive deterioration of visual fields. The optic nerve head is generally considered to be the primary site of axonal injury in glaucoma. Although the pathophysiology of glaucomatous optic neuropathy is not well understood, elevated intraocular pressure is considered the most important modifiable risk factor. However, in normal-tension glaucoma, intraocular pressure is not elevated and thus other risk factors must also be involved in the optic neuropathy of primary open-angle glaucoma. Several studies reported significantly lower intracranial pressure in patients with glaucoma compared with healthy subjects, suggesting that low intracranial pressure may result in a high pressure difference across the lamina cribrosa, influencing the physiology and pathophysiology of the optic nerve head by the effect of a mechanical force. Moreover, a rapidly evolving literature suggests the existence of an ‘ocular glymphatic system’. This opens up new ways to understand the mechanisms underlying a range of ocular diseases such as glaucoma. In the present paper, I hypothesize that an imbalance between intraocular pressure and intracranial pressure, apart from generating mechanical forces at the lamina cribrosa, may lead to a dangerous interplay between ocular fluid and cerebrospinal fluid resulting in impaired cerebrospinal fluid entry into the optic nerve subarachnoid space and optic nerve perivascular spaces, and the perivascular space surrounding the central retinal artery in particular, thereby inhibiting glymphatic clearance of waste products from the retrobulbar or retrolaminar portion of the optic nerve. Should further research demonstrate that the proposed viewpoint is largely correct, it would hold great potential for our understanding of glaucomatous optic nerve damage and would have important implications for diagnosis and therapy of this devastating disorder.

Transient visual field impairment after cold provocation in glaucoma patients with Flammer syndrome.

Background:It is still debatable whether visual field defects in glaucoma have a reversible component and to what extent a temporary loss can be provoked.Objective:To investigate the response of the visual function to a cold provocation in glaucoma patients, particularly to test whether subjects with Flammer syndrome (FS) behaved differently from subjects without FS.Methods:Ten (10) primary open-angle glaucoma (POAG) patients with FS, 7 POAG patients without FS, and 11 healthy controls were tested with program G2 on the Octopus 101 perimeter before and after putting one hand in cold water (4°C) for 2 min. The mean sensitivity (MS) of each visual field was included in the statistical analysis.Results:In glaucoma patients with FS, the mean MS significantly decreased after cold provocation (delta MS = –0.91 dB, CI = –1.43 to –0.39, p = 0.0014). In contrast, the mean MS in glaucoma patients without FS did not change significantly (delta MS = 0.17 dB, CI = –0.43 to 0.78, p = 0.56). Likewise, the mean MS did not change significantly in the healthy controls (delta MS = 0.23 dB, CI = –0.27 to 0.72, p = 0.36).Conclusions:Cold provocation induced a transient visual field deterioration in the glaucoma patients with FS but not in the glaucoma patients without FS or in the healthy controls. We assume this effect to be the result of a transient reduction of ocular blood flow.

Neuronal mechanisms of motion detection underlying blindsight assessed by functional magnetic resonance imaging (fMRI)

Brain imaging offers a valuable tool to observe functional brain plasticity by showing how sensory inputs reshape cortical activations after a visual impairment. Following a unilateral post-chiasmatic lesion affecting the visual cortex, patients may suffer a contralateral visual loss referred to homonymous hemianopia. Nevertheless, these patients preserve the ability to unconsciously detect, localize and discriminate visual stimuli presented in their impaired visual field. To investigate this paradox, known as blindsight, we conducted a study using functional magnetic resonance imaging (fMRI) to evaluate the structural and functional impact of such lesion in a 33-year old patient (ML), who suffers a complete right hemianopia without macular sparing and showing strong evidences of blindsight. We thus performed whole brain and sliced thalamic fMRI scan sequences during an event-related motion detection task. We provided evidence of the neuronal fingerprint of blindsight by acquiring and associating neural correlates, specific structures and functional networks of the midbrain during blindsight performances which may help to better understand this condition. Accurate performance demonstrated the presence of residual vision and the ability to unconsciously perceive motion presented in the blind hemifield, although her reaction time was significantly higher in her blind-field. When the normal hemifield was stimulated, we observed significant contralateral activations in primary and secondary visual areas as well as motion specific areas, such as the supramarginal gyrus and middle temporal area. We also demonstrated sub-thalamic activations within the superior colliculi (SC) and the pulvinar. These results suggest a role of secondary subcortical structures in normal spontaneous motion detection. In a similar way, when the lesioned hemifield was stimulated, we observed contralateral activity in extrastriate areas with no activation of the primary lesioned visual cortex. Moreover, we observed activations within the SC when the blind hemifield was stimulated. However, we observed unexpected ipsilateral activations within the same motion specific areas, as well as bilateral frontal activations. These results highlight the importance of abnormal secondary pathways bypassing the primary visual area (V1) in residual vision. This reorganization in the structure and function of the visual pathways correlates with behavioral changes, thus offering a plausible explanation for the blindsight phenomenon. Our results may potentially impact the development of rehabilitation strategies to target subcortical pathways.

Cost-effectiveness analysis of standalone trabecular micro-bypass stents in patients with mild-to-moderate open-angle glaucoma in Canada

Objectives: To estimate the cost-utility of two trabecular micro-bypass stents (TBS) implantation vs standard of care (SOC) in patients with mild-to-moderate open-angle glaucoma (OAG) in the Canadian healthcare setting.Methods: The deterioration in visual field (VF) defect over a 15-year time horizon was tracked using a Markov model with Hodapp-Parrish-Anderson stages of glaucoma (mild, moderate, advanced, severe/blind) and death as health states. Meta-analyses of randomized clinical trials were conducted to estimate the pooled reduction in intraocular pressure (IOP) and medication use due to TBS and SOC. The rate of decline in VF loss was adjusted by the extent of IOP reduction to estimate transition probabilities. Healthcare resource utilization, unit costs (2017 CAD), and progression-related utility scores were obtained by literature review, and medication costs with wastage were obtained from IMS Brogan PharmaStat. The impact of parameter and methodological uncertainty on costs and quality-adjusted life years (QALYs) was examined using probabilistic and 1-way sensitivity analyses.Results: The meta-analysis showed an additional reduction of 1.13 medications/patient and an additional decrease in IOP of –1.10 mmHg at 36 months favoring TBS. TBS strongly dominated medication alone, due to higher improvement in quality-of-life (0.068 QALYs), fewer blind eyes (–0.0031), and a decrease in total healthcare costs of C$2,908.3 per patient over the time horizon (C$9,394.1 TBS vs C$12,302.4 medication alone). Sensitivity analyses showed that results were robust to the uncertainties in model inputs and assumptions. Time-to-dominance was 44 months (3.7 years).Conclusions: The TBS procedure was cost-effective over SOC in a 15-year time horizon, with quality-of-life gains.

Using Vision to Study Poststroke Recovery and Test Hypotheses About Neurorehabilitation

Approximately one-third of stroke patients suffer visual field impairment as a result of their strokes. However, studies using the visual pathway as a paradigm for studying poststroke recovery are limited. In this article, we propose that the visual pathway has many features that make it an excellent model system for studying poststroke neuroplasticity and assessing the efficacy of therapeutic interventions. First, the functional anatomy of the visual pathway is well characterized, which makes it well suited for functional neuroimaging studies of poststroke recovery. Second, there are multiple highly standardized and clinically available diagnostic tools and outcome measures that can be used to assess visual function in stroke patients. Finally, as a sensory modality, the assessment of vision is arguably less likely to be affected by confounding factors such as functional compensation and patient motivation. Given these advantages, and the general similarities between poststroke visual field recovery and recovery in other functional domains, future neurorehabilitation studies should consider using the visual pathway to better understand the physiology of neurorecovery and test potential therapeutics.

Association between visual field impairment and involvement in motor vehicle collision among a sample of Japanese drivers

BackgroundThere is an expectation that the addition of visual field testing to driving licencing procedures may contribute to detecting unsafe drivers due to visual field (VF) impairment. However, previous research has been inconclusive as to the association between VF impairment and motor vehicle collision (MVC), and there are relatively fewer trials conducted outside the United States using a sample of general drivers compared to studies using eye clinic patients. PurposeTo investigate the association between ophthalmic indicators of VF impairment and involvement in at-fault MVC in the previous five years among a sample of middle-aged or older drivers. MethodDriving licence holders aged 40 years or over (N = 546) were administered a questionnaire survey and underwent a visual assessment at a driving licence examination centre in the suburbs of Tokyo. Of these participants, 458 were current drivers. Their response to the written questionnaire and ophthalmic indicators of VF impairment were subjected to multivariate logistic regression models to predict at-fault MVC. The analyses were done while adjusting for variables pertinent to driving habit, near-miss experience and perceived driving difficulties. We compared two different dependent variables separately: at-fault MVC based on police record and self-reports. ResultsAnalysis showed that ophthalmic indicators of binocular VF impairment such as Esterman score and Integrated Visual Field was not statistically significant in explaining at-fault MVC involvement. This was true both for predicting police-registered MVC and self-reported at-fault MVC. It was indicated that history of citation, presence of medical conditions and certain driving circumstances such as frequent night-time driving would increase risk of at-fault MVC in conjunction with the individual’s perception about driving difficulties. ConclusionThe results of this study were consistent with previous research in that ophthalmic VF impairment may not be directly associated with MVC involvement when VF impairment is not severe. However, a combination of at-risk driving behaviour (exposure to high-risk driving situations and certain near-miss experience), deterioration in health condition, and lack of insight into such circumstances would likely increase at-fault MVC risk.

Assessing driving risk in patients with glaucoma.

Glaucoma is the leading cause of irreversible blindness worldwide and can affect a broad array of daily activities, including driving. Recently, studies investigating the relationship between driving performance and glaucoma have received a great deal of interest. Assessment of driving behavior is not straightforward because driving is a complex skill involving significant multi-tasking ability. In this review, we summarize recent work from clinical studies investigating how glaucoma can affect driving performance. Patients with glaucoma are more likely to be involved in motor vehicle collisions when compared to healthy subjects. Here we describe how conventional functional tests performed in glaucoma patients, such as visual field measurements via standard automatic perimetry, are associated with driving performance. However, the risk of motor vehicle collisions is not entirely attributable to visual field impairment in glaucoma, suggesting that other factors also account for both driving safety and performance. Finally, we show different studies suggesting that parameters from driving simulators can be helpful because they can identify the impact of visual loss on complex situations.

Factors Associated with Progression of Japanese Open-Angle Glaucoma with Lower Normal Intraocular Pressure

To characterize the natural history and define the risk factors associated with the progression of normal-tension glaucoma (NTG) in Japanese patients who were followed up closely without treatment. Prospective 5-year study. Patients with NTG with intraocular pressure (IOP) consistently ≤15 mmHg without treatment at baseline. Visual field (VF) examinations were performed every 3 months, and disc/peripapillary retina photographs were taken every 6 months. Patients were followed up without treatment. Deterioration in VF was defined by reference to Guided Progression Analysis Software of the Humphrey VF Swedish Interactive Thresholding Algorithm 24-2 (Carl Zeiss Meditec, Jena, Germany) and disc/peripapillary retina deterioration as adjudged by 3 independent observers. Life table analysis was used for evaluating the time to disease progression, as defined by VF or deterioration of the optic nerve head structure. The Cox proportional hazards model was used to identify risk factors for glaucoma progression. We enrolled 90 patients (mean age, 53.9 years; baseline IOP, 12.3 mmHg; mean deviation [MD],-2.8 decibels [dB]). The MD slope averaged-0.33 dB/year (median,-0.23; 95% confidence interval [CI],-0.44 to-0.22). Glaucoma progression probability at 5 years was 66% (95% CI, 55-78), as defined by VF deterioration or disc/peripapillary retina deterioration (criterion 1): 52% (95% CI, 37-60), as defined by VF deterioration (criterion 2), and 50% (95% CI, 38-71), as defined by disc/peripapillary retina deterioration (criterion 3). Presence or history of disc hemorrhage (DH) (P < 0.001), long-term IOP fluctuation (P= 0.020), and a greater vertical cup-to-disc ratio (v-C/D) (P= 0.018) were significant predictors for progression defined by criterion 1. Long-term IOP fluctuation (P= 0.011) and a greater v-C/D (P= 0.036) were significant predictors for progression by criterion 2. Presence or history of DH (P= 0.0018) and long-term IOP fluctuation (P= 0.022) were significant predictors for progression by criterion3. In Japanese patients with NTG with mean baseline IOP of 12.3 mmHg without treatment, estimated mean MD slope for 5 years was -0.33 dB/year; probability of glaucoma progression based on VF or disc/peripapillary end points at 5 years was 66%. Presence or history of DH, long-term IOP fluctuation, and greater v-C/D significantly contributed to progression.

FIXED COMBINATIONS IN THE TREATMENT OF GLAUCOMA

Glaucoma is a slowly progressive neuropathy with changes in the optic nerve, the retinal neurofibrillar layer, and the field of vision.The aim of the paper is to present the significance of detecting elevated intra ocular pressure in early glaucoma detection.Glaucoma is one of the leading causes of blindness in the world. According to the latest WHO estimates, as a challenge to global level resolution - carcinomas are in the first place, cardiovascular diseases in second, and blindness in third place. The glaucoma accounts for about 9-12% of all blind people in the world, that is, this disease is diagnosed in about 2.5 million people each year. WHO predicts that the percentage will increase to 30% by 2020.The definition of the 2014 European Glaucoma Association (EEC 2014) reads: "Glaucoma is a chronic progressive optic neuropathy with characteristic morphological changes on the optic nerve disc and the retinal neurofibrillar layer as well as the progressive death of ganglia cells with visual field loss in the absence other eye diseases and congenital anomalies. " Hence, in addition to the standard methods available to us, such as measuring the height of the intraocular pressure (IOP), gonioscopy, eyelid examination, as well as determining and monitoring visual acuity, the necessity of the standard computerized perimetry and optic coherent tomography of back eye segment.Timely diagnosis of glaucoma is the only mechanism to combat this disease. The new methods offer a variety of new possibilities for investigating the earliest changes in the optic nerve disc and the retinal neurofibrillar layer. Their use should be combined with the classic glaucoma testing methods, such as standard computerized perimeter. But the basis is the early detection of an increased IOP by means of mass measurements with screening programs in risky or general groups. According to modern ophthalmic protocols, all patients with an increased IOP must be computed perimetrically once a year. In patients with significant changes in the field of vision, more often, for six months, the findings of the visible fields are compared. The new methods provide a quick, precise and timely diagnosis of this severe disease, which, if not detected, leads to safe blindness in time. Early combination therapy may be appropriate in patients with advanced glaucoma, patients with a high progression rate in patients with high IOP and / or severe visual field impairment, as well as in younger patients. Fixed combination therapy should be considered when patients fail to achieve their individualized IOP targets with monotherapy when 2 special applications of drops are preferred.

A Method to Measure the Rate of Glaucomatous Visual Field Change.

PurposeTo develop a method to measure the rate of glaucomatous visual field (VF) deterioration and to identify fast progressors.MethodsRetrospective, longitudinal, observational study of 8486 eyes of 4610 glaucomatous patients with ≥6 VFs and ≥3 years of follow-up. A Glaucoma Rate Index (GRI) was calculated. VF locations were partitioned into exponential decay or exponential improvement models. A pointwise rate of change (PRC) was estimated with an exponential fit and expressed as the percent/year change of the age- and location-matched normal perimetric range, presented as a spatially conserved VF map. PRCs were summed and normalized with boundary rates set by simulated decaying and improving VF series on a scale of −100 to +100, respectively.ResultsA total of 89,704 VF examinations with 425,039 test location series was used. Median follow-up and number of VFs/eye were 9.7 years and 9 VFs, respectively. Initial and final mean deviations (±SD) were −4.2 (±5.2) and −5.7 (±6.4) dB. The proportions of test locations designated as decayed, improved, and unchanged were 13%, 4%, and 83%, respectively. Mean PRCs for decay, improvement, and no change were −3.7 (±4.7)%/y, 2.5 (±2.6)%/y, and −0.5 (±2.1)%/y, respectively. The number of eyes with negative and positive GRIs was 5802 (68%) and 2390 eyes (28%), respectively. The proportion of eyes defined as fast progressors was 6.8%.ConclusionsGRI provides a robust measure of glaucomatous VF change, operates without discontinuity over the entire perimetric range, and can be used to identify fast progressors.Translational RelevanceThis study describes a novel method that can help the clinician to determine VF progression.

Evaluation of Structure-Function Relationships in Longitudinal Changes of Glaucoma using the Spectralis OCT Follow-Up Mode

The detection of glaucoma progression is an essential part of glaucoma management. Subjectivity of standard automated perimetry (SAP) prevents the accurate evaluation of progression, thus the detection of structural changes by optical coherence tomography (OCT) is attracting attention. Despite its objectivity, there is controversy about the appropriateness of the use of OCT, because many previous studies have indicated OCT results may not reflect the deterioration of visual field. A reason for this dissociation may be the test-retest variability of OCT, a major cause of which is misplacement of the measurement location. Recent advantages of spectral-domain OCT (SD-OCT), especially Spectralis OCT with an eye-tracking system (follow-up mode) enable measurement at approximately the same location as previous examinations. In addition to utilizing Spectralis follow-up mode, we introduced structure-function relationship map and nonlinear relationship between SAP and OCT results in considering structure-function relationship in longitudinal changes. The introduction of these two ideas in our study population improved the correlation between the SAP and OCT (R = 0.589 at most). The results of this study support the practical use of OCT in glaucoma progression but also stress the importance of focus on the corresponding focal changes and the consideration of disease severity.

Improving Spatial Resolution and Test Times of Visual Field Testing Using ARREST.

PurposeCorrectly classifying progression in moderate to advanced glaucoma is difficult. Pointwise visual field test–retest variability is high for sensitivities below approximately 20 dB; hence, reliably detecting progression requires many test repeats. We developed a testing approach that does not attempt to threshold accurately in areas with high variability, but instead expends presentations increasing spatial fidelity.MethodsOur visual field procedure Australian Reduced Range Extended Spatial Test (ARREST; a variant of the Bayesian procedure Zippy Estimation by Sequential Testing [ZEST]) applies the following approach: once a location has an estimated sensitivity of <17 dB (a “defect”), it is checked that it is not an absolute defect (<0 dB, “blind”). Saved presentations are used to test extra locations that are located near the defect. Visual field deterioration events are either: (1) decreasing in the range of 40 to 17 dB, (2) decreasing from >17 dB to “defect”, or (3) “defect” to blind. To test this approach we used an empirical database of progressing moderate-advanced 24-2 visual fields (121 eyes) that we “reverse engineered” to create visual field series that progressed from normal to the end observed field. ARREST and ZEST were run on these fields with test accuracy, presentation time, and ability to detect progression compared.ResultsWith specificity for detecting progression matched at 95%, ZEST and ARREST showed similar sensitivity for detecting progression. However, ARREST used approximately 25% to 40% fewer test presentations to achieve this result in advanced visual field damage. ARREST spatially defined the visual field deficit with greater precision than ZEST due to the addition of non–24-2 locations.ConclusionsSpending time trying to accurately measure visual field locations that have high variability is not productive. Our simulations indicate that giving up attempting to quantify size III white-on-white sensitivities below 17 dB and using the presentations saved to test extra locations should better describe progression in moderate-to-advanced glaucoma in shorter time.Translational RelevanceARREST is a new visual field test algorithm that provides better spatial definition of visual field defects in faster test time than current procedures. This outcome is achieved by substituting inaccurate quantification of sensitivities <17 dB with new spatial locations.

Current possibilities of visual rehabilitation

Diseases of the eyes and visual pathways can lead to different visual field defects, which limit the patients' abilities in everyday life in different ways. Central visual field defects cause mainly reading disorders and peripheral defects cause disorders of orientation and mobility. Rehabilitation measures have to be adapted specifically to the deficit and the individual needs of the patient. In central scotoma, reading ability can mostly be restored by magnifying visual aids. In reading disorders caused by insufficient size of the reading visual field, text magnification is contraindicated. In this case, contrast-enhancing or non-visual aids are applied. Modern electronic media are successfully used particularly by young people with visual impairments. Computer-based training programs are of increasing importance, especially saccadic training for orientation disorders due to concentric and homonymous visual field impairments.

A Rare Neurological Complication - Posterior Reversible Encephalopathy Syndrome in a Patient with Systemic Lupus Erythematosus and Class IV Lupus Nephritis

Abstract Posterior reversible encephalopathy syndrome is a rare manifestation of systemic lupus erythematosus, characterized by altered mental status, headache, convulsions, visual field impairment and posterior and reversible alterations on imaging scans(1,2). The clinical picture develops over a few hours, presenting with rapidly progressive neurological symptoms(3). It was first described in 1996. It is more frequent in patients with acute kidney injury or chronic kidney disease, thus in lupus patients with kidney disorders. It is associated with hypertension, other autoimmune diseases beside lupus, immunosuppressive therapies, especially antibody-based immunosuppressive therapy, and organ transplantation. It is clinically reversible within one week and imaging changes resolve within 2-4 weeks. It is treatable and has a good prognosis. We present the case of a young woman of 27 years, diagnosed with systemic lupus erythematosus who developed convulsive seizures, headache, visual impairment, being under immunosuppressive therapy with azathioprine. The kidney biopsy revealed class IV lupus nephritis and partial remission of the nephrotic syndrome. The other manifestations of SLE in this patient were cutaneous, immunological, articular and haematological. The patient had a good short, medium and long-term prognosis at 30 days and also at 6 months.

Gaze-Contingent Flicker Pupil Perimetry Detects Scotomas in Patients With Cerebral Visual Impairments or Glaucoma.

Background: The pupillary light reflex is weaker for stimuli presented inside as compared to outside absolute scotomas. Pupillograph perimetry could thus be an objective measure of impaired visual processing. However, the diagnostic accuracy in detecting scotomas has remained unclear. We quantitatively investigated the accuracy of a novel form of pupil perimetry.Methods: The new perimetry method, termed gaze-contingent flicker pupil perimetry, consists of the repetitive on, and off flickering of a bright disk (2 hz; 320 cd/m2; 4° diameter) on a gray background (160 cd/m2) for 4 seconds per stimulus location. The disk evokes continuous pupil oscillations at the same rate as its flicker frequency, and the oscillatory power of the pupil reflects visual sensitivity. We monocularly presented the disk at a total of 80 locations in the central visual field (max. 15°). The location of the flickering disk moved along with gaze to reduce confounds of eye movements (gaze-contingent paradigm). The test lasted ~5 min per eye and was performed on 7 patients with cerebral visual impairment (CVI), 8 patients with primary open angle glaucoma (age >45), and 14 healthy, age/gender-matched controls.Results: For all patients, pupil oscillation power (FFT based response amplitude to flicker) was significantly weaker when the flickering disk was presented in the impaired as compared to the intact visual field (CVI: 12%, AUC = 0.73; glaucoma: 9%, AUC = 0.63). Differences in power values between impaired and intact visual fields of patients were larger than differences in power values at corresponding locations in the visual fields of the healthy control group (CVI: AUC = 0.95; glaucoma: AUC = 0.87). Pupil sensitivity maps highlighted large field scotomas and indicated the type of visual field defect (VFD) as initially diagnosed with standard automated perimetry (SAP) fairly accurately in CVI patients but less accurately in glaucoma patients.Conclusions: We provide the first quantitative and objective evidence of flicker pupil perimetry's potential in detecting CVI-and glaucoma-induced VFDs. Gaze-contingent flicker pupil perimetry is a useful form of objective perimetry and results suggest it can be used to assess large VFDs with young CVI patients whom are unable to perform SAP.

Baseline Lamina Cribrosa Curvature and Subsequent Visual Field Progression Rate in Primary Open-Angle Glaucoma

To investigate the relationship between the degree of posterior bowing of the lamina cribrosa (LC) at baseline and the rate of subsequent visual field (VF) progression in eyes with primary open-angle glaucoma (POAG). Prospective, observational study. One hundred one early-stage (VF mean deviation [MD], -5.0 to -0.01 dB) POAG eyes that met the following conditions: (1) follow-up longer than 3.5 years, (2) more than 5 reliable standard automated perimetry tests, and (3) medically well-controlled intraocular pressure during follow-up. All participants underwent swept-source OCT scanning of the LC at baseline. The area enclosed by a vertical line at the anterior laminar insertion, anterior LC plane, and reference plane of Bruch's membrane opening (BMO) was divided by D (distance between the 2 cross-points made by vertical lines drawn from the anterior laminar insertion to the reference plane of BMO) to approximate the LC depth (LCD). The difference between the LCD and mean anterior laminar insertion depth was defined as the LC curvature index (LCCI). To consider the steepness of the LC curve, the adjusted LCCI (aLCCI) was calculated as LCCI divided by D and multiplied by 100. The mean LCD (mLCD), mean LCCI (mLCCI), and mean aLCCI (maLCCI) were computed by averaging the measurements on 12 radial scans. The subsequent MD slope and associated factors were analyzed. Lamina cribrosa parameters and subsequent MD slope. The participants' mean baseline MD was -3.8 ± 3.4 dB. The mean baseline mLCD, mLCCI, and maLCCI were 419.0 ± 111.2 μm, 76.4 ± 29.0 μm, and 4.8 ± 1.9, respectively. A greater MD slope was associated with a greater baseline maLCCI (P < 0.001). We found a statistically significant breakpoint for the maLCCI (4.12) above which a larger maLCCI showed a steeper MD slope (P < 0.001). Analysis by age revealed that significantly more VF progression with maLCCI changes occurred in the relatively younger group (≤69 years; P= 0.043). The baseline maLCCI showed a significant correlation with the rate of subsequent VF deterioration. This suggests that, in POAG eyes with greater posterior bowing of the LC, the axons of retinal ganglion cells may be more vulnerable to further glaucomatous injury.