Inferior Arcuate Defect Research Articles

Clinical Correlates of Computationally Derived Visual Field Defect Archetypes in Patients from a Glaucoma Clinic

ABSTRACTPurpose: To assess the clinical validity of visual field (VF) archetypal analysis, a previously developed machine learning method for decomposing any Humphrey VF (24-2) into a weighted sum of clinically recognizable VF loss patterns.Materials and Methods: For each of 16 previously identified VF loss patterns (“archetypes,” denoted AT1 through AT16), we screened 30,995 reliable VFs to select 10–20 representative patients whose VFs had the highest decomposition coefficients for each archetype. VF global indices and patient ocular and demographic features were extracted retrospectively. Based on resemblances between VF archetypes and clinically observed VF patterns, hypotheses were generated for associations between certain VF archetypes and clinical features, such as an association between AT6 (central island, representing severe VF loss) and large cup-to-disk ratio (CDR). Distributions of the selected clinical features were compared between representative eyes of certain archetypes and all other eyes using the two-tailed t-test or Fisher exact test.Results: 243 eyes from 243 patients were included, representative of AT1 through AT16. CDR was more often ≥ 0.7 among eyes representative of AT6 (central island; p = 0.002), AT10 (inferior arcuate defect; p = 0.048), AT14 (superior paracentral defect; p = 0.016), and AT16 (inferior paracentral defect; p = 0.016) than other eyes. CDR was more often < 0.7 among eyes representative of AT1 (no focal defect; p < 0.001) and AT2 (superior defect; p = 0.027), which was also associated with ptosis (p < 0.001). AT12 (temporal hemianopia) was associated with history of stroke (p = 0.022). AT11 (concentric peripheral defect) trended toward association with trial lens correction > 6D (p = 0.069).Conclusions: Shared clinical features between computationally derived VF archetypes and clinically observed VF patterns support the clinical validity of VF archetypal analysis.

Multifocal Electroretinogram and Fundus Autofluorescence Findings in Acute Zonal Occult Outer Retinopathy during a Three- Year Follow-Up

Acute zonal occult outer retinopathy is a disease difficult to diagnose. Within this pathology, many clinical and para-clinical tests appear normal regardless the great advances in technology. However, the findings we discovered with electrophysiology when paired with a thorough clinical anamnesis are the more reliable parameters for giving the right diagnosis.We present a clinical case of a 26 year old patient with diagnosis of acute zonal occult outer retinopathy whose optical coherence tomography and fluorescein angiography results were normal while the results of the wide field electroretinogram and multifocal electroretinogram showed alterations in the outermost layers of the retina which correlated with inferior arcuate defect in the visual field and peri-macular areas of hyperautofluorescence in the auotofluorescence. The evolution of the case is shown during 3 years appreciating the disappearance of the autofluorescence as well as progressive improvement in the visual field.

Clinical Reasoning: A 42-year-old man with sequential monocular visual loss

In April 2005, a 42-year-old African American man developed insidious, painless visual loss in the left eye which quickly progressed over several weeks. There was no significant medical history. Family history revealed hypertension and diabetes, but no autoimmune disorders, brain tumors, or vision loss. He was a restaurant manager, smoked ½ pack of cigarettes daily, consumed alcohol rarely, and did not use illicit drugs. He presented to another institution, where he was found to have 20/100 acuity, dyschromatopsia, and a relative afferent pupillary defect in the left eye. The left optic nerve head was mildly swollen, without hemorrhage or exudate. Humphrey visual fields of the left eye revealed a dense superior altitudinal defect with a less prominent inferior arcuate defect. The right eye field was full. He was thought to have idiopathic optic neuritis. He was treated briefly with oral corticosteroids, but his vision in the left eye never improved. ### Questions for consideration: 1. What are the diagnostic considerations for subacute monocular visual loss in an adult? 2. What diagnostic workup would you perform? The differential diagnosis for subacute monocular visual loss is broad. Although idiopathic demyelinating optic neuritis is a common cause, the differential also includes inflammatory and infectious conditions, compression, infiltrative or neoplastic processes, hereditary optic neuropathies, glaucoma, retinal disorders, and ischemic optic neuropathy (table 1). View this table: Table 1 Differential diagnosis for subacute monocular visual loss ### Optic neuritis. Optic neuritis most often occurs between the ages of 20 to 50 and is three times more frequent in women.1 Visual loss reaches its nadir within 7 to 10 days and begins to recover within 1 month. Retro-orbital pain, particularly with eye movements, occurs in almost all cases; it may precede the visual loss and typically persists for 1 to 2 weeks.2 Characteristic findings on examination support the diagnosis of typical optic neuritis. Visual field …

Juxtapapillary Capillary Hemangioblastoma

Juxtapapillary capillary hemangioblastomas are vascular lesions that occur on the optic nerve head or immediately adjacent to the optic disc. Although juxtapapillary capillary hemangioblastomas may appear as an isolated clinical finding, they are more likely to be a precursor to the diagnosis of von Hippel-Lindau (VHL) disease. When associated with VHL, the ocular complications from hemangioblastoma are generally greater, and subsequently the prognosis is poorer than for isolated entities. A 67-year-old white male presented to our clinic complaining of decreased vision in both eyes at distance and near. A dilated fundus examination revealed a swollen left optic nerve. Visual field testing revealed an inferior arcuate defect in the left eye. Laboratory and radiological testing were normal. Fluorescein angiography showed filling during the retinal arterial phase with late diffuse leakage. Based on these results, a diagnosis of juxtapapillary capillary hemangioblastoma was made. This was later confirmed when fundus photographs taken 7 years earlier were obtained, revealing a stable appearance to the nerve. Potential ocular complications of juxtapapillary capillary hemangioblastomas include vision loss secondary to subretinal and intraretinal fluid, as well as epi-retinal membrane formation and, rarely, exudative retinal detachment. Management ranges from observation to surgical intervention, although definitive treatment guidelines have yet to be established. In addition, it is important for the eye care practitioner to be aware of the association with VHL disease, so that patients may be appropriately referred and managed for other possible systemic complications of the disease.

Muslin-induced intracranial sterile abscess: A cause of visual loss after aneurysm repair

Report of a Case A68-year-old white woman developed acute onset of severe headache in 1982. Computed tomography (CT) scans of the head revealed a subarachnoid hemorrhage, and cerebral angiography demonstrated a left paraophthalmic artery aneurysm. The patient underwent aneurysm clipping, with wrapping of the base with muslin. Three weeks after surgery the patient noted mild blurred vision of the left eye. Visual acuity was 20/20 in both eyes, and there was optic disc pallor in the left eye (OS). Goldmann visual field testing was full for both eyes (OU). The patient remained visually stable for several years. In 1990, she developed painless loss of vision in the left eye. Visual acuity was 20/20 OU and there was a trace afferent pupillary defect OS; Goldmann visual field examination was full OD and revealed an inferior arcuate defect OS. CT scan of the head demonstrated “postsurgical changes only” and a diagnosis of “anterior ischemic optic neuropathy” OS was made. In August 1996, the patient was referred to the neuro-ophthalmology service at Baylor College of Medicine with painless progressive loss of vision OS over the previous 2 years. Visual acuity was 20/20 in the right eye (OD) and count fingers OS. Again, there was an afferent pupillary defect and optic atrophy OS. Visual field testing showed a superotemporal defect OD and a central island OS. Cerebral angiography did not reveal an aneurysm. CT scan of the head showed a ring-enhancing mass in the parasellar region (Figure 1). The patient underwent craniotomy and, at surgery, a cystic mass was identified. The mass contained a “cheesy-like” material with several pieces of muslin floating freely within the cavity. The results of Gram stain and culture of this material were negative. Surgical decompression with excision and drainage of the mass was performed. Histopathological examination of the mass revealed dense areas of scarring and a polymorphic infiltrate composed of lymphocytes, plasma cells, neutrophils, and numerous lipid-laden histiocytes. Multiple foci of necrosis with microabscesses were present. Under polarized light, scattered birefringent foreign bodies were observed (Figure 2). Foci of epithelioid histiocytes and multinucleated giant cells were also noted. At last follow-up visit in February 1997, the patient’s vision was 20/20 OD and 3/200 OS. Visual field examination remained unchanged.