Onset Of Visual Field Defects Research Articles

Branch Retinal Artery Occlusions, Paracentral Acute Middle Maculopathy and Acute Macular Neuroretinopathy After COVID-19 Vaccinations.

PurposePotential retinal adverse events after COVID-19 vaccinations reported previously include paracentral acute middle maculopathy (PAMM), acute macular neuroretinopathy (AMN), and central serous chorioretinopathy. We report four cases of branch retinal artery occlusion (BRAO), one case of PAMM, and one case of AMN that occurred after administration of the Pfizer-BioNTech COVID-19 vaccine.Patients and MethodsWe retrospectively reviewed the medical records of six patients who presented to Yame General Hospital or Oita University Hospital from July through October 2021.ResultsFour patients (2 males) presented with visual field defects associated with BRAO, one male patient with PAMM, and one female patient with AMN after receiving the Pfizer-BioNTech COVID-19 vaccine. The mean age was 59.3 years; the mean best-corrected visual acuity was 20/21. The mean time from the last vaccination to the onset of visual field defect was 22.8 days. Five patients had received two doses of the vaccine and one patient one dose. Patients’ medical history included diabetes mellitus in case 2, hypertension in cases 2, 3 and 6, and Alport syndrome and end-stage renal disease in case 6 for which the patient was undergoing regular hemodialysis.ConclusionAlthough rare, retinal adverse events may occur after COVID-19 vaccinations. Further studies with a larger sample size should determine whether these retinal abnormalities are causally associated with COVID-19 vaccinations or just coincidental. Potential risks of BRAO/PAMM/AMN after COVID-19 vaccinations must be carefully weighed against the substantial benefit of COVID-19 vaccinations.

Trousseau's syndrome caused by bladder cancer producing granulocyte colony-stimulating factor and parathyroid hormone-related protein: A case report.

The present study reports a rare case of bladder cancer that caused Trousseau's syndrome, a malignancy-associated hypercoagulative state leading to venous or arterial thrombosis. A 38-year-old Japanese female patient experienced a sudden onset of visual field defects and lower limb weakness. Cerebral magnetic resonance imaging revealed multi-regional hypointense areas compatible with acute cerebral infarction. Despite the repeated administration of anticoagulant treatment with heparin, the condition could not be adequately controlled and thromboembolic events occasionally recurred. Several tumor markers, including carbohydrate antigen 19-9, cancer antigen 125, carcinoembryonic antigen, cytokeratin 19 fragment and squamous cell carcinoma antigen levels, were elevated. Consequently, computed tomography scans were performed, which revealed a massive bladder tumor with multiple bone and lymph node metastases. The patient also exhibited other paraneoplastic disorders, including leukocytosis due to granulocyte colony-stimulating factor (G-CSF) production, and hypercalcemia due to parathyroid hormone-related protein (PTHrP) production. Transurethral resection of the bladder tumor was performed, and the tumor was pathologically confirmed as urothelial cell carcinoma. Immunohistochemical testing revealed positive staining for G-CSF and PTHrP. Despite undergoing gemcitabine/cisplatin-based systemic chemotherapy, the disease developed rapidly and the patient succumbed to the disease within 3 months of initial symptoms. The present case indicates that occult visceral malignancy should be considered in patients with unexplained thromboembolism.

Acute-Onset Altitudinal Visual Field Defect Caused by Optic Canal Meningioma

Dear Editor, Altitudinal visual field defect (VFD), which involves the loss of visual sensation in the horizontal half of the visual field, is caused mainly by anterior ischemic optic neuropathy (AION),1,2,3 or rarely by compressive neuropathy due to a tumor or aneurysm.4,5 However, acute-onset inferior altitudinal VFD is a hallmark of AION.1,2,3 We observed a patient with a rapidly developed inferior altitudinal VFD due to a small meningioma inside the optic canal, which was almost undetectable in standard imaging studies. A 65-year-old man with hypertension and hyperlipidemia complained of blurred vision persisting over several days. He denied having headache, diplopia, or ocular pain. He had a history of medullary infarction and was taking aspirin, antihypertensive medication, and a statin. With the exception of the old infarction, there were no abnormal findings on axial T2-weighted MRI scans obtained 10 months previously (Supplementary Fig. 1 in the online-only Data Supplement). An ophthalmologic examination revealed decreased visual acuity in the left eye (10/20) compared to the right (16/20). Humphrey perimetry revealed an inferior altitudinal VFD in the left eye, which was more severe on the nasal side than on the temporal side (Fig. 1A). There was no evidence of relative afferent pupillary defects, ptosis, proptosis, or disc swelling, or pallor on funduscopy. Ocular movement, intraocular pressures, and slit-lamp and optical coherence tomography findings were normal. The acute onset and painless monocular visual loss raised a suspicion of AION, leading to a focus on evaluating the patient's vascular etiology. However, there were no abnormal findings on MR angiography (Supplementary Fig. 1 in the online-only Data Supplement). A follow-up visual field test performed 3 weeks later revealed an aggravated altitudinal VFD, especially on the inferior temporal side (Fig. 1A). High-spatial-resolution (2-mm slice thickness) MRI with gadolinium enhancement of the orbit was performed to exclude compressive neuropathy mimicking AION. The results revealed a 1.2-cm meningioma on the posterior part of the left optic canal causing medial displacement and downward compression of the optic nerve (Fig. 1B and C). The patient underwent a frontotemporal craniotomy and resection of the meningioma. The tumor originated from the left side tuberculum sellar and extended into the optic canal. Although he reported a subjective improvement in vision immediately after surgery, the VFD was aggravated on the superior side just before surgery (Fig. 1A). Four months after resection of the tumor, his vision had partially recovered (Fig. 1A). Fig. 1 Serial Humphrey perimetries and high-resolution MRI of compressive optic neuropathy with a monocular inferior altitudinal visual field defect (VFD). A: Initial Humphrey perimetry shows an inferior altitudinal VFD in the left eye that is more severe on ... The main mechanism underlying the visual disturbance in compressive optic neuropathy is secondary disruption of the axoplasmic flow and demyelination of the optic nerve.6 Therefore, the onset of VFD usually progresses slowly. Since the optic nerve delivers visual information received from each of the retinal quadrants to the optic chiasm, the VFD can present in various patterns according to the initial direction of optic nerve compression. In this case the VFD started at the inferonasal area and extended to the inferotemporal area, which can be explained by a medial downward displacement of the optic nerve due to compression from the meningioma (Fig. 1D). The VFD was rapid and severe due to the meningioma being located on the optic canal and the diagnosis delay. Another possible mechanism is ischemia caused by vascular compression. Ischemic symptoms usually present as posterior ischemic optic neuropathy (PION) with compression of the collateral branches from the ophthalmic artery in the optic canal.7 However, ischemia is unlikely to be the main mechanism in this case for two reasons: 1) an altitudinal VFD is relatively rare in PION7 and 2) in this case the VFD worsened according to the direction of nerve compression and improved following surgical resection. Other features associated with compressive optic neuropathy were absent in this case, which may be due to the smallness of the tumor. Optic nerve meningioma arising within the optic canal is rare.8 These tumors are usually extremely small despite causing significant visual disturbance and can easily be overlooked on routine MRI. Furthermore, they may not have any orbital signs, and may present with a normal-appearing optic disc.8 Therefore, it is necessary to consider compressive optic neuropathy when a patient presents with an altitudinal VFD, even in the absence of other symptoms.

Early Visual Symptom Patterns in Inherited Retinal Dystrophies

The present retrospective study compared initial visual symptom patterns in inherited retinal dystrophies (IRD) on the basis of records of 544 patients diagnosed with a wide variety of IRD at the Tuebingen University Eye Hospital from 2005 to 2008. Age at first onset of symptoms was noted, and the following clinical data were analyzed: visual acuity (VA), night vision disturbances, photophobia, onset of visual field defects, best corrected VA, and types of visual field defects. Median age at visual symptom onset was defined with 25th and 75th percentiles and compared in 15 IRD types. The main trends in VA changes in retinitis pigmentosa and cone-rod dystrophies were identified. This study was the first to combine disease history and clinical data analysis in such a wide variety of IRD. It showed that patterns of initial symptoms in IRD can provide extra clues for early differential diagnosis and inclusion of IRD patients in clinical trials.

Branch Retinal Artery Embolization Due to Calcific Aortic Valve Stenosis

Branch retinal artery occlusion caused by calcific embolization secondary to calcific aortic valvulopathy. A 45-year-old woman came to our attention complaining a sudden painless loss of her peripheral superior visual field. Best visual acuity was 20/20. Fundus examination revealed the presence of a retinal arterial embolic occlusion of the inferior branch. Fundus retinography, visual field, and fluorescein angiography were performed and medical therapy was started. The echocardiography examination revealed a tricuspid and calcified aortic valve with moderate stenosis and regurgitation. Due to the heart pathology, the patient moved to the cardiosurgery department, where an aortic valve replacement was performed. Four months after cardiac surgery, visual acuity of both eyes was stable (20/20). Fundus examination showed a complete reabsorption of the retinal edema and the resolution of retinal pallor. Fluorescein angiography confirmed the delay of the arterial filling. No retinal ischemia was observed. The visual field examination confirmed the deep scotoma previously registered. Retinal arterial embolization is a rare but potentially devastating complication of calcific aortic stenosis. Initial retinal presentation of calcific aortic stenosis is a rare condition. Keeping in mind that these emboli may be recurrent and potentially bilateral, a sudden onset of visual field defects, especially in young asymptomatic patients, needs immediate diagnosis and consideration of an urgent surgical correction.

Foveal Color and Luminance Sensitivity Losses in Glaucoma

Losses in color vision sensitivity are noted in patients with glaucoma and these losses can occur before the onset of visual field defects in ocular hypertensive patients. The authors incorporate a technique that measures foveal luminance and isoluminant-color thresholds. This study included 31 patients with glaucoma, 10 patients suspected of having glaucoma, and 67 control subjects. The testing conditions measured thresholds under identical spatial and temporal conditions. Individual differences in luminosity between colors were controlled by presenting 16 different ratios of the three phosphors on a color monitor. Relative to the control subjects, the patients with glaucoma showed a nonselective defect in both color and luminance sensitivity for red-green stimuli (P < .05), but a selective color defect for yellow-blue stimuli (P < .01). There were no statistically significant differences between patients suspected of having glaucoma and control subjects (P > 0.3). If the isoluminant-color stimuli are detected by foveal P-ganglion cells, then these results suggest that glaucoma leads to a generalized decrease in P-ganglion cell sensitivity that is more pronounced for cells with an input from cones sensitive to short wavelengths.

Nachweis progredienter glaukomatöser Papillenveränderungen vor dem Auftreten von Gesichtsfelddefekten

Computerized disc analysis was used for the longitudinal monitoring of patients with moderate intraocular pressure elevation. 44 patients (80 eyes) were monitored for at least 18 months; 25 patients (47 eyes) were monitored for at least 12 months; 15 patients (25 eyes) were monitored for at least 18 months. On average, one computerized disc analysis was performed every 4 months. Eight eyes showed a progressive decrease in their neuroretinal rim area. Seven of them were monitored for more than 18 months, one was monitored for 15 months. In all cases, the progressive decrease in neuroretinal rim area was significant, p less than or equal to .1. It is non-physiological and has to be interpreted as a serious sign of ongoing glaucoma damage. In addition, it obviously precedes the onset of visual field defects. Seven out of 8 eyes with progressive decrease in their neuroretinal rim area have normal visual fields up to now. In one case a progressive decrease in neuroretinal rim area was found at first and small visual field defects developed subsequently.

Correlation of color vision deficits and observable changes in the optic disc in a population of ocular hypertensives.

Both glaucomatous cupping and the presence of acquired color vision deficits have been reported to be precursors to the onset of visual field defects in patients with suspected glaucoma. To examine the relationship between early glaucomatous cupping and acquired color vision anomalies, we performed anomaloscope (Pickford-Nicholson) and Farnsworth-Munsell 100-Hue color vision tests in 48 ocular hypertensive eyes with either clinical evidence of early glaucomatous cupping (group 1) or no evidence of glaucomatous cupping (group 2). All patients had normal visual fields, as determined by extensive static perimetry of the central visual field and kinetic perimetry of the peripheral visual field. Although the overall incidence of blue and blue-green color vision anomalies in the ocular hypertensives was comparable with that reported in previous studies, we found no clear association between early glaucomatous cupping and color vision anomalies. The relationship between these two precursors to visual field loss remains unclear.

Ocular pressure and visual fields. A ten-year follow-up study.

In general, an association exists between the ocular pressure level and the future development of glaucomatous visual function loss. Using the ocular pressure reading, the task of searching for individuals who are likely to develop glaucomatous visual function loss can be limited. Identification of the individual who is destined to develop glaucomatous field defect cannot be made on the basis of tonometric and tonographic values with any practical degree or precision as to warrant the diagnosis or the therapeutic intervention for glaucoma prior to the onset of visual field defect, nor can the definite diagnosis of glaucoma be made in the individual subject prior to the demonstration of a characteristic involvement of visual function. Skillful thorough examination of the central visual field must be the cornerstone of any attempt at early detection of glaucoma.