Bilateral Reduction In Visual Acuity Research Articles

Occult macular dystrophy: brief literature review

Occult macular dystrophy is characterized by a slowly progressive bilateral reduction of visual acuity in patients with normal fundus and fluorescein angiography. We describe a case of a 36-year-old male patient diagnosed with this condition, after extensive investigation with multimodal imaging, electrophysiology tests, and systemic screening. Occult macular dystrophy: brief literature review

Visual Functional Limitation in Amblyopia: A Review

Amblyopia is a unilateral or bilateral reduction in visual acuity in absence of any pathological causes. It results in limitations of various visual functions including visual acuity that are essential for performing daily living activities. In this study, we conducted a comprehensive review of affected visual functions in amblyopia through a Pubmed search with an extensive search strategy. Seventeen research articles were selected out of 420 possible research articles and included in the study. Besides visual acuity, other visual functions such as contrast sensitivity, fixation stability, accommodative functions, visuomotor behavior, binocularity, stereopsis, and visual attention were found to be significantly affected in amblyopia. Interestingly, the visual functions corresponding to the "normal eye" of the amblyopic patients were also found to be significantly affected in all forms of amblyopia.

Clinical features, diagnosis and management of serpiginuos choroiditis

Classic serpiginous choroiditis (CSC) is a rare bilateral, multifocal, recurrent inflammatory disease of the choroid and retina observed mainly in young and middle-aged male patients. We present three cases of otherwise healthy men (ages 30, 52, and 54 years) with the diagnosis of CSC based on clinical and multimodal imaging findings. During the observation period, slow progression of the fundus changes was noted in each patient despite various individualized immunosuppressive treatments (corticosteroids, cyclosporin, cyclophosphamide, azathioprine) used. Progressive macular involvement was associated with a significant irreversible bilateral reduction in visual acuity. The aim of the study is to present the clinical features of CSC, possible diagnostic and therapeutic options, and to familiarize the reader with specific clinical cases.

English

BACKGROUND The term amblyopia literally means dullness of vision. It is defined as unilateral or bilateral reduction of visual acuity due to pattern vision deprivation or abnormal binocular interaction for which no ocular causes can be detected by ocular examination and can be reversed by therapeutic measures. The study was undertaken to estimate the proportion of non-compliance and factors affecting it in children undergoing occlusion therapy for amblyopia. METHODS The study was designed as a hospital based cross sectional study. Children aged 5 - 12 years undergoing occlusion therapy for amblyopia due to strabismus, anisometropia or both, who had been prescribed occlusion for a period of minimum 3 months were included in the study. Children with developmental or neurological disorders and other ocular conditions causing visual impairment, whose parents were not willing to participate in the study or follow up, and uncooperative children were also excluded from the study. RESULTS 52.5 % were non-compliant to occlusion therapy, 31.1 % were partially compliant and only 16.4 % were compliant. 38.5 % had final visual acuity in the range of 6 / 60 - 6 / 24 and 6 / 18 – 6 / 12, 20 % had 6 / 9 - 6 / 6. Different variables were assessed against compliance to check for any association. Significant association was found between compliance to occlusion and socioeconomic status (p = .006), visual acuity at presentation (p = .026), type of amblyopia (p = .038) and final visual acuity (p < .01) and association with educational status were found to be borderline (p = .059). CONCLUSIONS Occlusion therapy for amblyopia is a long drawn process which needs strict compliance and regular follow up. Compliance is a major factor affecting final visual outcome. Poor compliance leads to unsuccessful amblyopia therapy which in turn can have negative impact on child’s learning ability and psychosocial wellbeing. For this reason it is critical that care givers leave the clinic with clear knowledge of how and why patching is being recommended and its importance in improving child’s vision. KEYWORDS Amblyopia, Occlusion, Compliance

Acquired dyschromatopsia in acute myelocytic leukaemia

Patients with haematological malignancy are referred to the ophthalmologist either with visual symptoms or to exclude orbital or intraocular involvement after the diagnosis has been established. This report describes a patient with acute myelocytic leukaemia (AML) whose presenting symptom was dyschromatopsia. A 52-year-old female, previously in good health, presented with a disturbance of colour vision. On examination, there was bilateral reduction in visual acuity, impaired colour vision and severely constricted visual fields. Electrophysiological testing and colour contrast sensitivity (CCS) assessment were performed. CCS showed bilateral threshold elevation in the tritan axis of both eyes, right worse than left. Pattern ERG showed marked macular dysfunction in the right eye, but was normal in the left eye. Full-field ERGs fell within the normal range. Pattern VEPs were reduced in the right eye, without peak time shift; flash VEPs showed bilateral delay. Investigation showed severe anaemia, and a bone marrow biopsy confirmed a diagnosis of acute AML. There was symptomatic improvement in visual acuity and colour vision following blood transfusion and initiation of chemotherapy. This appears to be the first case report of dyschromatopsia in AML with symptomatic improvement following treatment. The case lends support to previously suggested hypotheses of chromatic visual disturbance in association with presumed hypoxia.

The island of ischaemia: submacular choroidal nonperfusion in giant cell arteritis

Sir, Olali et al1 presented a case of biopsy-proven giant cell arteritis (GCA) with atypical visual loss. The visual impairment had manifested as bilateral reduction of visual acuity but with sparing of peripheral field. Fluorescein angiography provided the denouement: there was focal perfusion defect localised to the submacular choroid. The angiographic curiosity was more pronounced in the right eye, with its central scotoma of greater eminence, as evidenced by a poorer acuity. The authors noted that this pattern—of isolated focal ischaemic choroidopathy in GCA patients—had been reported earlier.2 However, as the literature burgeons we become ever remiss of treasures from the past. Almost 40 years ago a monograph called ‘Segmental nature of the choroidal vasculature' appeared in the British Journal of Ophthalmology, a masterclass by SS Hayreh on the anatomy and haemodynamics of the choroidal vascular system, with allusion to the superimposition of diseases including arteritis.3 A homage to this contribution better explains the features observed by Olali et al1 in their patient. They wished specifically to report ‘pigmentary disturbance' at the maculae in a case of GCA in whom there appeared no other ophthalmoscopic features. A reference to the oeuvre of Hayreh affords insight: acute submacular choroidal ischaemia causes pallor of the overlying retinal pigment epithelium. Eventually, the pallid zone acquires depigmentation, the precise ophthalmoscopic anomaly visible in the patient under discussion. Indeed the description appended by Olali et al1 to their case report can be elevated to a formulation in dilgenter: in their presented arteritic case, the occurrence of submacular ischaemia (with sparing of the optic nerve head) denoted hypoperfusion in the lateral posterior ciliary artery (LPCA), the vascular stalk that serves the temporal posterior choroid. As perfusion pressure decreased inside the LPCA—in this situation as consequence of arteritis—the submacular choroid was the first casualty of ischaemia because it is a watershed vascular territory. This is the explanatory nub of the clinical constellation detected in this patient. Of further intrigue, the optic nerve head escaped infarction because it retained perfusion from the medial PCA and a meshwork of circumferential short PCAs. With unsuppressed disease progression, however, the inevitable course would have been arteritic anterior ischaemic optic neuropathy, as the operational nerve head feeders succumbed finally to arteritis. Through a marshalling of superb diagrams, the outstanding duo of McLeod and Hayreh,4 both now emeritus professors, have earlier expounded the behaviour of the choroidal tree as observed after piecemeal cauterisation of its various feeder PCAs. Also in this patient, the submacular choroidal ischaemia was cast into a sharp outline by the 19-s image from the angiogram. Later, at 52 s, the outermost fringe of the ischaemic zone had turned indistinct. Explanation for this observation again comes from the experiments of landmark stature, which hark back some 40 years. As ischaemic patches form within the choroid there is remedial response from neighbouring vascular systems, instanced among others by retrograde flux in the vortex veins. When such zones of choroidal ischaemia are captured over days and weeks via serial angiograms, the non-perfused zones are seen to contract in area. The speed of angiographic filling improves through brisk consolidation of collateral flow. Thus, late frames were found to show dye ingress into choroidal zones that showed stark ischaemia in the opening sequence. The broader message for ophthalmologists is that, in its incipient stealthy phase, GCA can produce localised ischaemic patches in the choroid while entirely sparing the optic nerve and retinal arterial system. Ophthalmologists must be cognizant of this possibility when faced with an older patient who has seemingly inexplicable visual loss and biomicroscopic signs of minimal intensity.

Electrophysiological and Histologic Assessment of Retinal Ganglion Cell Fate in a Mouse Model forOPA1-Associated Autosomal Dominant Optic Atrophy

The main disease features of autosomal dominant optic atrophy (ADOA) are a bilateral reduction of visual acuity, cecocentral scotoma, and frequently tritanopia, which have been ascribed to a progressive loss of retinal ganglion cells (RGCs) and subsequent degeneration of the optic nerve. The main disease-causing gene is OPA1. Here, we examine a mouse carrying a pathogenic mutation in Opa1 by electrophysiological measurements and assess the fate of RGCs. Two-year-old animals underwent a full examination by electroretinography (ERG) and visually evoked potential (VEP) measurements to assess the function of the outer and inner retina and the optic nerve. Retrograde Fluorogold labeling was performed to determine the number of surviving RGCs and to assess axonal transport by neurofilament counterstaining. Phagocytosis-dependent labeled microglial cells were identified by an Iba-1 staining. ERG responses were normal in aged Opa1 mice. VEP measurements revealed significantly reduced amplitudes but no change in the latencies in contrast to extended latencies found in glaucoma. Retrograde labeling of RGCs showed a significant reduction in the number of RGCs in Opa1 mice. Long-term experiments revealed the presence of microglial cells with ingested fluorescent dye. This is the first electrophysiological demonstration of a visual function deficit in aged Opa1 mice. VEP measurements and retrograde labeling experiments show that the number of RGCs is reduced whereas the remaining RGCs and axons function normally. Taken together, these findings support an ascending progress of degeneration from the soma toward the axon.

Subtle neurological and metabolic abnormalities in an Opa1 mouse model of autosomal dominant optic atrophy

The ubiquitously expressed gene OPA1 is the main disease causing gene for autosomal dominant optic atrophy (ADOA). These patients present with bilateral reduction in visual acuity, central visual field defects and impaired color vision, secondary to the progressive loss of retinal ganglion cells (RGCs) and subsequent degeneration of the optic nerve. Up to now, it is not clear why a mutation in a ubiquitously expressed gene affects only RGCs and the optic nerve. Twenty-two-month-old Opa1 animals underwent a full examination following the Shirpa protocol. Weight, food intake and life span were monitored. Rotarod treadmill experiments were performed to assess neuromuscular function. Limb skeletal muscle was evaluated morphologically, mitochondrial cytochrome c oxidase (COX) activity was studied histochemically and mtDNA integrity was determined by long-range PCR. The Shirpa test showed that 33% of the Opa1 mice suffered from tremor and 52% of the Opa1 animals showed an abnormal clutching reflex. Control animals performed well in the accelerating Rotarod treadmill experiment whereas the Opa1 mice performed significantly worse. Skeletal muscle fibers were morphologically normal, had normal COX activity and showed no evidence of secondary mtDNA damage in contrast to patients with syndromic ADOA. We also found a highly significant difference in body weight. Our results demonstrate that OPA1 mutations affect not only RGCs but also other tissues and cell types, though to a lesser extent. In particular we found deficits in both neuromuscular and metabolic function. We therefore want to encourage clinicians to be vigilant about to extra-ocular manifestations in ADOA patients.

Pseudoangiitis bei beidseitiger okulärer Ischämie

The term 'frosted branch angiitis' was initially used to describe an idiopathic form of vasculitis in association with panuveitis. It has since also been used to describe the angiographic phenomenon of diffuse leakage along retinal vessels against the background of other ocular and systemic diseases. We describe a 57-year-old male patient with acute bilateral reduction of visual acuity, headaches and absence of any pulse at the temporal arteries. Fluorescence angiography showed bilateral diffuse leakage along all the retinal vessels, which resembled frosted branches. Laboratory parameters and histology were not indicative of vasculitis. Imaging showed complete occlusion of both common carotid arteries and a hypoplastic vertebral artery on the left. Ocular ischemia may imitate primarily inflammatory conditions in its angiographic appearance.

Bilateral, Persistent Serous Macular Detachments With Waldenstr??m???s Macroglobulinemia

Waldenström's macroglobulinemia is a rare, malignant lymphoplasmacytic disorder characterized by the monoclonal proliferation of immunoglobulin type M (IgM) producing B-lymphocytes. Ocular manifestations of Waldenström's macroglobulinemia have been described in association with the conjunctiva, cornea, uvea, retina, and periocular adnexa. Only rarely have macular findings, particularly serous macular detachments, been described in the presence of monoclonal hypergammaglobulinemias. The majority of reports to date have documented resolution of these serous macular detachments after treatment with blood plasmapheresis. This report presents a case of bilateral, persistent serous macular detachments in the presence of Waldenström's macroglobulinemia. A 53-year-old black man presented with gradual bilateral reduction in visual acuity over the last 2 months. He revealed having been diagnosed with Waldenström's macroglobulinemia approximately 1 month before presentation. He also reported having undergone multiple plasmapheresis treatments in conjunction with systemic chemotherapy over the same period. Funduscopic and fluorescein angiographic examination revealed bilateral, serous macular detachments in the presence of mild venous stasis retinopathy secondary to serum hyperviscosity. Subsequent funduscopic evaluations and serial optical coherence tomography readings confirmed the persistence of the serous detachments despite multiple plasmapheresis treatments. Although the funduscopic manifestations of excess serum immunoglobulins are typically the sequelae of circulatory stasis, the serum hyperviscosity induced in Waldenström's macroglobulinemia has been shown on rare occasions to induce serous macular detachments. Physical elimination of the excess macroglobulins through plasmapheresis is quite effective in resolving the neurosensory detachments induced by Waldenström's macroglobulinemia. Only a fraction of neurosensory detachments resulting from Waldenström's macroglobulinemia persist despite multiple plasmapheresis treatments. Novel angiographic evidence of retinal pigment epithelium atrophy beneath the area corresponding to the serous detachment provides a plausible explanation for unresponsive nature of this presentation. Identification of this rare variant of the classic angiographically silent macula known to occur with Waldenström's macroglobulinemia can aid the clinician in determining a patient's potential response to plasmapheresis and their final visual prognosis.

A multicenter, randomized, double-blind, crossover study of patient preference for tadalafil 20 mg or sildenafil citrate 50 mg during initiation of treatment for erectile dysfunction

Background: Tadalafil is a phosphodiesterase 5 (PDE5) inhibitor approved in >30 countries for the treatment of erectile dysfunction (ED). It has been shown to improve erectile function compared with placebo in Phase III studies, but clinical experience comparing tadalafil with the PDE5 inhibitor sildenafil citrate is lacking. Objective: This study compared patient preference for tadalafil 20 mg or sildenafil 50 mg during initial treatment for ED. It also compared the tolerability of the 2 agents at these doses. Methods: This randomized, double-blind, fixed-dose, 2-period crossover trial took place at 13 sites in the United States and Germany. Patients were randomized 1:1 to receive 4 weeks of treatment with tadalafil 20 mg or sildenafil 50 mg, followed by the alternative treatment, to be taken as needed up to once daily before sexual activity. Results: The study enrolled 215 men with ED, 109 randomized to the tadalafil-sildenafil sequence and 106 to the sildenafil-tadalafil sequence. Their mean age was 49.8 years; 84.7% were sildenafil naive and 15.3% had undergone a previous inadequate trial of sildenafil. Most patients had moderate ED (60.5%) of ≥1 year's duration (74.9%). Of 190 evaluable patients, 126 (66.3%) preferred to initiate treatment with tadalafil, compared with 64 (33.7%) with sildenafil ( P < 0.001). Patients' preference did not differ by age, duration of ED, treatment sequence, or previous sildenafil exposure. Both medications were well tolerated, with no significant differences in the incidence of treatment-emergent adverse events. Headache (11.2% tadalafil, 8.8% sildenafil), dyspepsia (6.0% and 4.2%, respectively), nasopharyngitis (4.7% and 2.8%), and flushing (2.8% and 4.7%) were the most common adverse events. The rate of ocular disturbances was low: 1 patient experienced intermittent bilateral reduction in visual acuity with tadalafil, and 2 exhibited conjunctival hyperemia or eyelid edema with sildenafil. Conclusions: Tadalafil 20 mg was preferred to sildenafil 50 mg for the initiation of ED therapy in this study population. Both medications were well tolerated.

Bilateral central retinal artery occlusions in a patient with activated protein C resistance

We describe the case of a 42‐year‐old woman who had two episodes of visual loss, first in one and later in the other eye, which caused bilateral reduction of visual acuity to 2/10 with optic atrophy. Detailed clinical and laboratory assessment revealed an activated protein C (APC) resistance and no other obvious cause. APC resistance has not been previously reported as an etiologic factor of central retinal artery occlusion.

Vision and refraction of school children

Abstract Even though prophylactic medical examination of children has been carried out in Denmark since 1947, measurement of visual acuity in young children was not performed systematically until the National Health Service issued instructions making sight testing a major part of the 4 year medical examination. If this has had an effect, it should now be possible to record a fall in the number of school children with amblyopia as a result of anomalies of refraction and strabismus.The present investigation comprises all the children, who attended int the 2nd to 5th classes during the school year 1983/84, in schools in the municipality of Odense. 8769 school medical files were examined and 1216 children selected for supplementary eye examination. The remainder had normal vision without glasses. 1034 of those examined had an anomaly of refraction or reduced vision from other causes.97% of all the eyes had a visual acuity of 6/6. The frequency of children with unilateral vision ≤6/12, and who did not suffer from eye disease, comprised 1.07%. There were statistically significantly more boys (1.39%) than girls (0.73%) with amblyopia. Thus, there is a fall in the number of amblyopic children in relation to previous Danish investigations. Bilateral reduction in visual acuity ≤6/18 was found in 0.09%; this has not changed to any greater extent during the last decades.Myopia was found in 4.0% of the children between the ages of 7–11 years. compared to previous studies no change was observed in the younger ages and modest rise in the older age groups. The onset of myopia occurred earlier in girls (9–10 years) than in boys (11 years). This may, in part, explain why myopia was seen in 4.4% of the girls and only in 3.6% of the boys. Severe myopia (&gt;/6.0 D) was found in 13 children (18 eyes) corresponding to a frequency of 0.15%.

A case of isoniazid-induced optic neuropathy

A case of optic neuropathy induced by combined isoniazid and rifampin treatment is reported. The patient was a 61-year-old woman with a tuberculous abscess of the lung. She was treated with isoniazid (8.5–20 mg/kg/day, total dosage about 120 g) and rifampin (15 mg/kg/day, total dosage about 81 g) for approximately six months. At the end of this time, raised levels of glutamate oxalacetate transaminase and glutamate pyruvate transaminase were seen with peripheral sensory neuropathy. Rifampin was discontinued. Two months later, optic neuropathy also developed. Bilateral reduction of visual acuity, a central scotoma and abnormality of color vision were observed. Isoniazid was withdrawn and treatment by pyridoxine (vitamin B,) was initiated. Complete recovery of the optic neuropathy as well as the peripheral neuropathy was seen ten months after the withdrawal of isoniazid.