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Visual Loss (visual + loss)
Kinds of Visual Loss Selected AbstractsClinicopathological Conference: 29-year-old with Visual Loss, Hypertension, and a SeizureACADEMIC EMERGENCY MEDICINE, Issue 9 2007Jeffrey R. Suchard MD First page of article [source] 4343: What next when the biopsy is negative in suspected giant cell arteritis (GCA)?ACTA OPHTHALMOLOGICA, Issue 2010A BOSCHI Purpose To present and discuss the approach of GCA when temporal artery biopsy (TAB) is negative. Recommendations for reducing the rate of negative TAB Methods GCA is the commonest vasculitis. Visual loss occurs in up to one-fifth of patients, which may be preventable by prompt recognition and treatment. Features predictive of ischaemic neuro-ophthalmic complications are: jaw claudication, diplopia, and temporal artery abnormalities on physical examination. These manifestations and particularly blindness and jaw claudication seems to be more commonly associated with positive TAB. Results Despite visual symptoms TAB may result negative. Rate of negative TAB varies from 7% to 40% in pat suspected of GCA. TAB should be done 2 to 6 weeks after commencement of treatment, and at least 1 cm. Contralateral biopsy is controversies, usually it increases the rate of GCA diagnosis of only 5%. Conclusion If TAB is still however negative, but clinical suspicion high or Ultra-Sound suggests GCA or complications typical of GCA, like anterior ischemic optic neuropathy, patient should be treat as biopsy-positive GCA patient. If the clinical suspicion is low, features considered atypical or alternative explanations available, rapid glucocorticoid therapy should be tapered. [source] 4222: Potential retinal causes: when and how to investigateACTA OPHTHALMOLOGICA, Issue 2010BP LEROY Purpose To describe the retinal conditions that need to be excluded when non-organic visual loss is suspected, and the investigations required to either confirm or exclude them. Methods A case presentation format will be used to illustrate those conditions which can be discovered using psychophysical and electrophysiological tests as well as special imaging including autofluorescence, infrared and red free imaging and spectral-domain optical coherence tomography, in patients in whom a non-organic origin for visual loss is suspected. Results Inherited retinal diseases such as Stargardt macular dystrophy, X-linked retinoschisis and cone dystrophy as well as Batten disease in their early stages all need to be excluded when visual loss is thought to be non-organic. In addition, several acquired retinal conditions such as acute acular neuroretinopathy need to be taken into account. visual field testing, ISCEV-standard full-field flash electroretinography, pattern electroretinography and visual evoked potentials and specialised imaging techniques contribute significantly to making the correct diagnosis. Conclusion Visual loss in a list of organic conditions may mimic non-organic visual loss. Functional testing as well as specialised imaging techniques are essential in differentiating true organic from non-organic visual loss. [source] AML with bilateral retinal detachmentACTA OPHTHALMOLOGICA, Issue 2007E SARKADY Purpose: To present a case of thrombotic ocular and CNS involvement complicating acute myeloid leukaemia (AML). Methods: A 42 year old woman developed blurred vision shortly after diagnosis and treatment of M6 AML. Investigations showed anterior orbital infiltration, retinal detachment and panuveitis. Iris biopsy and vitreous aspirate were negative. She developed right temporal lobe infarction and died following further CNS infarction two months after initial diagnosis. Results: Post mortem examination showed cerebral oedema, multiple cerebral infarctions and hepatosplenomegaly; both eyes contained vitreous exudates, retinal detachment and uveal thickening. Microscopy showed exudative and haemorrhagic retinal detachment, without inflammatory or neoplastic infiltrate, and bilateral uveal leukaemic infiltration with infarction. Neoplastic cells infiltrated the leptomeninges and brain parenchyma with focal vascular occlusion. Lung vessels were occluded by neoplastic cells. The spleen and bone marrow were heavily infiltrated. Partial immunophenotyping suggested a diagnosis of acute promyelocytic leukaemia (APL). Conclusions: Acute leukaemia involves the eye occurs in 39-53% cases. Visual loss is uncommon. Retinal involvement most frequently occurs in the form of superficial haemorrhages, detachment is uncommon. Acute lymphoblastic leukaemia (ALL) treated with L-asparaginase, acute promyelocytic leukaemia (APL) and non-M3 AML may present with a prothrombotic state which may be catastrophic, as occurred in this fatal case. [source] Visual loss despite anticoagulation in radiation-induced optic neuropathyCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2004Helen V Danesh-Meyer FRANZCO Abstract Radiation therapy to the brain may produce necrosis and loss of function months after completion of the treatment. The case is presented of a 62-year-old man who developed radiation-induced optic neuropathy 2 years after treatment for a glioma of the left temporal lobe, despite being on anticoagulation therapy. Although anticoagulation appears to be beneficial in cerebral radiation necrosis, its usefulness in the treatment of radiation-induced optic neuropathy is unclear. [source] Cerebral arteriovenous malformation presenting as visual deterioration in a childDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2000Lesley C Kaye MRC Ophth Associate Specialist in Ophthalmology A rare case of visual loss as the presenting feature of a central arteriovenous malformation involving the vein of Galen is reported. A 5-year-old girl with a history of deteriorating vision for the past 6 months was examined. Ocular examination showed a left hemianopia, left optic atrophy, and dilated vessels of the right optic disc. MRI revealed a massive deep-seated central arteriovenous malformation involving the vein of Galen. The mechanism of visual loss is likely to be a combination of ischaemic optic atrophy associated with a steal phenomenon and direct compression of the right optic radiation. [source] Tongue Necrosis in Temporal ArteritisHEADACHE, Issue 8 2007Maria Goicochea MD Temporal arteritis is a form of systemic vasculitis that involves branches of the carotid artery. Clinical features are headache, visual loss, ophthalmoplegia, jaw claudication, temporal headache, with tenderness and thickening on the affected temporal artery. We present 3 cases of tongue necrosis due to this granulomatous arteritis. Ischemic necrosis of the tongue is unusual and appears to be an association between its occurrence and high dose steroid tapering. [source] Ethnic variation in AMD-associated complement factor H polymorphism p.Tyr402His,HUMAN MUTATION, Issue 9 2006Michael A. Grassi Abstract Age-related macular degeneration (AMD) is the most common cause of irreversible visual loss in the developed world. Previous studies have demonstrated that the c.1204T>C, p.Tyr402His allelic variant in the complement factor H (CFH) gene is associated with an approximately three-fold increased risk for AMD in Caucasians of predominantly European descent. Both the prevalence as well as the phenotypic spectrum of AMD varies widely among persons of different ethnicities. We hypothesized that populations with a lower prevalence of AMD might also have a lower prevalence of the CFH risk allele. In this study we sought to determine the frequency of this sequence variant in control populations of Caucasians, African Americans, Hispanics, Somalis, and Japanese. Normal control populations were assembled for each ethnic group: Caucasian (n=148), Somali (n=128), African American (n=75), Hispanic (n=81), and Japanese (n=82). Individuals were genotyped using a restriction digest assay and the frequency of the C allele at nucleotide position 1204 of the CFH gene was determined. A bioinformatic approach was used to identify SNPs in linkage disequilibrium with rs1061170 (c.1204T>C, p.Tyr402His) from the human haplotype map project database (HapMap) in order to validate the findings. We found widely discordant frequencies of the risk allele between some of the different ethnic groups: Japanese 0.07±0.02, Hispanics 0.17±0.03, African-Americans 0.35±0.04, Caucasians 0.34±0.03, and Somalis 0.34±0.03. Allele frequencies generated by analysis of the HapMap database were consistent with these findings. This study suggests that there are other yet unidentified genetic factors important in the pathogenesis of AMD that may mitigate the effects of c.1204T>C, p.Tyr402His variant. Hum Mutat 27(9), 921,925, 2006. © 2006 Wiley-Liss, Inc. [source] USH2A Mutation analysis in 70 Dutch families with Usher syndrome type II,,HUMAN MUTATION, Issue 2 2004Ronald J.E. Pennings Abstract Usher syndrome type II (USH2) is characterised by moderate to severe high-frequency hearing impairment, progressive visual loss due to retinitis pigmentosa and intact vestibular responses. Three loci are known for USH2, however, only the gene for USH2a (USH2A) has been identified. Mutation analysis of USH2A was performed in 70 Dutch USH2 families. Ten mutations in USH2A were detected, of which three are novel, c.949C>A, c.2242C>T (p.Gln748X) and c.4405C>T (p.Gln1468X). Including 9 previously published Dutch USH2a families, estimates of the prevalence of USH2a in the Dutch USH2 population were made. Mutations were identified in 62% of the families. In 28% both mutated alleles were identified, whereas in 34% the mutation in only one allele was found. It is estimated that about 28% of the Dutch USH2 families have a different causative gene. Analysis of deduced haplotypes suggests that c.1256G>T (p.Cys419Phe) is a Dutch ancestral mutation, occurring in 16% of the alleles. © 2004 Wiley-Liss, Inc. [source] Systemic lupus erythematosus complicated with posterior reversible encephalopathy syndrome and intracranial vasculopathyINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2010Hung-An CHEN Abstract Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic condition characterized by reversible vasogenic edema on neuroimaging. It is associated with various neurological manifestations, including headaches, vomiting, seizures, visual loss, altered mental status and focal neurological deficits. PRES mainly occurs in the setting of eclampsia, hypertension, uremia, malignancy, transplantation, autoimmune diseases and/or use of immunosuppressive drugs. This syndrome has been described in patients with systemic lupus erythematosus (SLE). PRES is a potentially reversible clinical,radiological entity; however, it can be complicated with vasculopathy, infarction or hemorrhage. Vasculopathy has been demonstrated to be a common finding in patients with SLE. We report the case of a woman with lupus nephritis and PRES whose diffuse vasculopathy was present on initial neuroimaging. Subsequent brain computed tomography scan demonstrated interval development of intraparenchymal hemorrhage and subarachnoid hemorrhage. To our knowledge, this unique brain image pattern has not been reported in SLE patients. [source] Wilson's disease presenting with rapidly progressive visual loss: Another neurologic manifestation of Wilson's disease?JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2001Paul J Gow Abstract Wilson's disease (WD) is a rare autosomal recessive disorder of copper metabolism resulting in copper-induced tissue damage that primarily involves the liver and central nervous system. The neurologic manifestations of WD almost universally involve a derangement of basal ganglia function or psychiatric disturbance. We report the case of a 46-year-old man presenting with end-stage liver disease caused by WD who had associated rapidly progressive optic neuropathy. We also discuss the possible association between the two conditions. [source] Perceived blur in amblyopiaOPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 6 2002A. J. Simmers Purpose:, It is well documented that visual acuity and contrast sensitivity in amblyopia are attenuated at high spatial frequencies: this would predict that amblyopes should perceive objects as blurred because they lack high spatial frequency information necessary to adequately represent sharp edges. In a series of experiments, we explored the representation of blur in amblyopia with blur discrimination and blur matching tasks. Methods:, Monocular blur discrimination thresholds were measured in a spatial 2-Alternative Force Choice procedure. The luminance profiles of the blurred edge were cumulative Gaussians with the standard deviation of the reference blurred edge being fixed at 1.88, 3.75, 7.5, 15, 30, or 60 min arc. Observers were required to discriminate which edge (right or left) appeared to be the less blurred. Observers also interocularly matched edges which were identical to those employed in the blur discrimination tasks, with the exception that they were viewed dichoptically at all times. Results:, Blur discriminination thresholds were elevated in both the amblyopic and fellow fixing eye but were within the normal range for interocular matching thresholds. Our results suggest that blur is veridically represented in the amblyopic visual system. Conclusions:, The surprising result here is that all amblyopes, even those with the most severe visual loss, veridically matched all blurred edges, including the sharpest ones. This implies that amblyopes are able to represent levels of blur that are defined by spatial structure beyond their resolution limit. These results also raise interesting questions about the mechanism by which blur is represented in the visual system. [source] Two cases of monocular visual loss during oral arsenic trioxide therapy of acute promyelocytic leukemia,AMERICAN JOURNAL OF HEMATOLOGY, Issue 10 2009Wing-Yan Au No abstract is available for this article. [source] Early Onset Childhood Cicatricial Pemphigoid: A Case Report and Review of the LiteraturePEDIATRIC DERMATOLOGY, Issue 2 2010Monia Kharfi M.D. We describe a new case in a 20-month-old boy, who is to our knowledge the youngest patient reported yet. The disorder had begun 10 months before he was referred to our department by mucosal crusted erosions of the oral and nasal cavities and conjunctivae. Cutaneous examination showed buccal erosions with limited mouth opening, entropion of the lower eyelids, trichiasis, cicatricial cornea, synechia of the nasal cavities and hypopigmented lesions of the abdomen. There were no anal or genital lesions. Cicatricial pemphigoid was confirmed by positive direct and indirect immunofluorescence on mucous biopsy. Systemic corticosteroids (2 mg/kg/day), maintained for 12 months, had led to complete healing of lesions. But due to cicatrization, synechia of the nasal cavities and corneal opacities, leading to a dramatic visual loss, have occurred. Dapsone 25 mg/day and topical ocular cyclosporine are now maintained to avoid relapse. Our review of the literature of all cases of CP showed that ocular and to a less degree, vulvar lesions are the most severe ones, due to the serious complications with scar formation. [source] Risk factors for visual impairment registration due to diabetic retinopathy in Leeds, 2002,2005PRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 3 2009Diabetes & Endocrinology, H Hayat Specialist Registrar Abstract We undertook a retrospective study of case notes of those patients registered blind or partially sighted due to diabetic retinopathy in the Leeds metropolitan area in the years 2002 and 2005. Both the incidence of visual impairment due to diabetic retinopathy and the relative contribution to total registrations are similar to those observed in other local and national studies. The main risk factors for registered visual impairment were poor glycaemic control prior to ophthalmic review, no prior retinopathy screening, late presentation with symptomatic visual loss, non-compliance with planned review and laser treatment failure. Most of these risk factors are avoidable. Nearly two-thirds of patients diagnosed with diabetes mellitus were being screened for diabetic retinopathy. These figures would suggest that the National Service Framework for Diabetes' proposed coverage of 80% by 2006 and 100% by the end of 2007 is achievable. The duration of diagnosed diabetes mellitus at the time of registration was an average of 16 years in this study. This reflects the slow development of sight-threatening retinopathy and visual loss observed previously. Conventional therapy for diabetic retinopathy with laser photocoagulation reduces the risk of visual loss more effectively than it improves visual function. Despite the increased risk of early worsening of retinopathy seen with intensive glycaemic control in the Diabetes Control and Complications Trial and the UK Prospective Diabetes Study, improved control closer to the time of diagnosis of diabetes mellitus would have helped to provide a sustained reduction in the risk of retinopathy developing or progressing. Both laser treatment failure and non-attendance may limit the benefits of improved screening coverage. Copyright © 2009 John Wiley & Sons. [source] Protein kinase C inhibition in diabetic retinopathy and microvascular diseasePRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 5 2007Dr C Walton FRCP Abstract Protein kinase C (PKC) activation by hyperglycaemia may play an important role in the evolution of diabetic retinopathy and other microvascular complications. The PKC-, inhibitor ruboxistaurin belongs to a new class of drugs and has been studied in several clinical trials in microvascular disease, the outcomes of which are described in this review. Ruboxistaurin exhibits promise as the first oral treatment shown to reduce visual loss and the need for laser treatment for macular oedema in patients with moderate to severe non-proliferative diabetic retinopathy. Copyright © 2007 John Wiley & Sons. [source] Longitudinal study of vision and retinal nerve fiber layer thickness in multiple sclerosisANNALS OF NEUROLOGY, Issue 6 2010Lauren S. Talman BA Objective Cross-sectional studies of optical coherence tomography (OCT) show that retinal nerve fiber layer (RNFL) thickness is reduced in multiple sclerosis (MS) and correlates with visual function. We determined how longitudinal changes in RNFL thickness relate to visual loss. We also examined patterns of RNFL thinning over time in MS eyes with and without a prior history of acute optic neuritis (ON). Methods Patients underwent OCT measurement of RNFL thickness at baseline and at 6-month intervals during a mean follow-up of 18 months at 3 centers. Low-contrast letter acuity (2.5%, 1.25% contrast) and visual acuity (VA) were assessed. Results Among 299 patients (593 eyes) with ,6 months follow-up, eyes with visual loss showed greater RNFL thinning compared to eyes with stable vision (low-contrast acuity, 2.5%: p < 0.001; VA: p = 0.005). RNFL thinning increased over time, with average losses of 2.9,m at 2 to 3 years and 6.1,m at 3 to 4.5 years (p < 0.001 vs 0.5,1-year follow-up interval). These patterns were observed for eyes with or without prior history of ON. Proportions of eyes with RNFL loss greater than test-retest variability (,6.6,m) increased from 11% at 0 to 1 year to 44% at 3 to 4.5 years (p < 0.001). Interpretation Progressive RNFL thinning occurs as a function of time in some patients with MS, even in the absence of ON, and is associated with clinically significant visual loss. These findings are consistent with subclinical axonal loss in the anterior visual pathway in MS, and support the use of OCT and low-contrast acuity as methods to evaluate the effectiveness of putative neuroprotection protocols. ANN NEUROL 2010;67:749,760 [source] Endothelial nitric oxide synthase gene polymorphisms in giant cell arteritisARTHRITIS & RHEUMATISM, Issue 11 2003Carlo Salvarani Objective To examine potential associations of the Glu/Asp298 polymorphism in exon 7 and the 4a/b polymorphism in intron 4 of the endothelial nitric oxide synthase (eNOS) gene with susceptibility to and clinical expression of giant cell arteritis (GCA), particularly in patients with versus those without ischemic complications. Methods Ninety-one consecutive patients with biopsy-proven GCA, who were residents of Reggio Emilia, Italy, and 133 population-based controls from the same geographic area were genotyped by polymerase chain reaction and allele-specific oligonucleotide techniques for eNOS polymorphisms in exon 7 and intron 4. The patients were separated into 2 subgroups according to the presence or absence of ischemic complications (visual loss and/or jaw claudication and/or aortic arch syndrome). Results The distribution of the Glu/Asp298 genotype differed significantly between GCA patients and controls (corrected P [Pcorr] = 0.003). Carriers of the Asp298 allele (Asp/Asp or Glu/Asp) were significantly more frequent among the GCA patients than among the controls (Pcorr = 0.0002, odds ratio 3.3, 95% confidence interval 1.7,6.3). The distribution of the 4a/b genotype was similar in GCA patients and controls. No significant associations were found when GCA patients with and without ischemic complications were compared. Conclusion Our findings show that the Glu/Asp298 polymorphism of the eNOS gene is associated with GCA susceptibility. [source] Retinal photography for diabetic retinopathy screening in Indigenous primary health care: the Inala experienceAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 2010Geoffrey K. P. Spurling Abstract Objective: We aimed to determine the impact of clinic based retinal photography on access to appropriate screening for diabetic retinopathy (DR). Design, setting and participants: We opportunistically recruited patients undergoing their annual diabetic cycle of care over a two year period in the urban Indigenous primary health care clinic. Data were collected on retinal outcomes, health variables and referral patterns. Main outcome measures: Access to appropriate screening and ophthalmic follow up, prevalence of DR, acceptability and feasibility of clinic-based retinal photography were the main outcome measures of this study. Results: One hundred and thirty-two of a possible 147 patients consented to participate. 30% of participants had DR. Appropriate screening and ophthalmic follow up increased six fold, from 20 to 124 participants, following the introduction of the retinal camera. Most participants felt very positive about DR screening. Conclusions: Primary care DR screening using retinal photography can improve access to DR screening for indigenous patients, reduce the burden on busy outpatient departments and should reduce visual loss. Policy-makers could contribute to screening sustainability by funding a medicare item-number for primary care based DR screening associated with the annual diabetic cycle of care. An upfront Practice Incentive Program (PIP) payment could offset set up costs. [source] Sight-threatening varicella zoster virus infection after fludarabine treatmentBRITISH JOURNAL OF HAEMATOLOGY, Issue 4 2000Y. L. Chee Varicella zoster virus (VZV) infection involving the posterior segment of the eye after fludarabine treatment has not previously been described. Two patients, who had completed fludarabine treatment 3 and 18 months previously, presented with visual loss that had been preceded by a recent history of cutaneous zoster. The use of the polymerase chain reaction (PCR) for VZV DNA from ocular specimens allowed rapid confirmation of clinical diagnosis and treatment with a good outcome in one patient. With the increasing use of fludarabine and other purine analogues, an awareness of such complications is important because of their potentially sight-threatening consequences. [source] Visual recovery in a man with the rare combination of mtDNA 11778 LHON mutation and a MS-like disease after mitoxantrone therapyACTA NEUROLOGICA SCANDINAVICA, Issue 4 2002C. Buhmann Buhmann C, Gbadamosi J, Heesen C. Visual recovery in a man with the rare combination of mtDNA 11778 LHON mutation and a MS-like disease after mitoxantrone therapy. Acta Neurol Scand 2002: 106: 236,239. © Blackwell Munksgaard 2002. We describe a young man with prognostic unfavourable homoplasmatic mitochondrial DNA(mt DNA) 11778 Leber's hereditary optic neuropathy (LHON) point mutation and confirmed multiple sclerosis (MS). This combination of LHON and MS-like disease is rare in both sexes, and in men has been described in only a few case reports. In a 4-year follow-up during immunosuppressive therapy with mitoxantrone, we found a remarkable time delayed visual recovery 12 months after acute onset of rapid sequential bilateral subtotal visual loss followed by episodes of isolated acute demyelinative optic neuropathy. Visual recovery to such extent after this latency is uncommon in both mtDNA 11778 LHON mutation and optic neuritis (ON) in MS. Relapses in visual deterioration must be considered as extremely rare in LHON. This case might support the hypothesis of an immunological pathogenetic factor in combined LHON and MS, and possibly in LHON alone. We suggest a search for the LHON mutation in MS patients with predominant visual impairment, independent of patients' gender. [source] 1363: White dot syndromesACTA OPHTHALMOLOGICA, Issue 2010S ANDROUDI Purpose The white dot syndromes (WDS) are a group of distinct clinical entities characterized by one common underlying feature: the presence of multiple "spots" in the fundus, usually in the deep retina or choroid without any other systemic manifestations. Methods The disorders are relatively rare and include the following entities: acute posterior multifocal placoid pigment epitheliopathy (APMPPE), multiple evanescent white dot syndrome (MEWDS), birdshot retinochoroidopathy (BSRC), serpiginous choroidopathy (SC), multifocal choroiditis and panuveitis (MCP), punctate inner choroidopathy (PIC), subretinal fibrosis and uveitis syndrome, and presumed ocular histoplasmosis syndrome (POHS). Results Despite the fact that many infectious and noninfectious inflammatory diseases may present with multifocal chorioretinal lesions, the entities included in the WDS share some features which make them a particular group of ocular disorders. In fact, the WDS would be better labeled as idiopathic inflammatory multifocal chorioretinopathies, since with the exception of diffuse unilateral subacute neuroretinitis, their causes are still unknown. Conclusion Because the specific diagnosis may have profound implications on therapy and prognosis, it is important to narrow the diagnosis to the greatest extent possible, even in patients with seemingly atypical findings. The correct diagnosis of WDS is important because the management is totally different from one another. Some of them are self-limited and have good visual outcomes without treatment, while others are associated with serious retinal and choroidal sequelae, which can result in severe visual loss even after adequate immunosuppressive therapy. [source] 1243: Missing subtle signsACTA OPHTHALMOLOGICA, Issue 2010A KAWASAKI Purpose To highlight some easily overlooked clinical findings which may be the key to arriving at the correct diagnosis. Methods Case studies Results Patient with unexplained visual loss, patient with oscillopsia, patient with red eye Conclusion Recognition of subtle clinical findings is an important skill that improves with effort and experience on the part of the clinician Commercial interest [source] 4341: Are visual evoked potentials and pattern ERG useful in neuro-ophthalmology?ACTA OPHTHALMOLOGICA, Issue 2010GE HOLDER Purpose To describe the roles of VEP and PERG in clinical neuroophthalmology. Methods Case based examples. Results Objective visual system testing with electrophysiology allows the distinction between optic nerve and macular dysfunction, often difficult in clinical practice. Examples will be shown of the types of VEP abnormality that can occur in different disorders of optic nerve function. PERG should also be performed in the patient with visual symptoms; if the PERG suggests macular dysfunction, full-field ERG is indicated in order to determine whether that macular dysfunction is part of a generalised retinal process or is dysfunction localised to the macula. Electrophysiology further allows the diagnosis of non-organic visual loss and the quantification of visual system dysfunction. Conclusion The objective functional assessment with electrophysiology is an important part of the diagnostic armamentarium available to neuroophthalmologists. [source] 4221: The initial consultation: when should non-organic visual loss be suspected?ACTA OPHTHALMOLOGICA, Issue 2010W SPILEERS Purpose When a patient reports visual loss and the doctor can not immediately find the etiology, a non-organic visual loss has to be excluded. Methods Different testing methods can be of value in deciding on organic versus non-organic visual loss: visual acuity and visual field measurements, pupillary reflexes, electrophysiologic testing, imaging techniques, ... Results The value of these different methods will be discussed and illustrated Conclusion The investigation of possible non-organic visual loss is a complex task [source] 4222: Potential retinal causes: when and how to investigateACTA OPHTHALMOLOGICA, Issue 2010BP LEROY Purpose To describe the retinal conditions that need to be excluded when non-organic visual loss is suspected, and the investigations required to either confirm or exclude them. Methods A case presentation format will be used to illustrate those conditions which can be discovered using psychophysical and electrophysiological tests as well as special imaging including autofluorescence, infrared and red free imaging and spectral-domain optical coherence tomography, in patients in whom a non-organic origin for visual loss is suspected. Results Inherited retinal diseases such as Stargardt macular dystrophy, X-linked retinoschisis and cone dystrophy as well as Batten disease in their early stages all need to be excluded when visual loss is thought to be non-organic. In addition, several acquired retinal conditions such as acute acular neuroretinopathy need to be taken into account. visual field testing, ISCEV-standard full-field flash electroretinography, pattern electroretinography and visual evoked potentials and specialised imaging techniques contribute significantly to making the correct diagnosis. Conclusion Visual loss in a list of organic conditions may mimic non-organic visual loss. Functional testing as well as specialised imaging techniques are essential in differentiating true organic from non-organic visual loss. [source] 4224: The role of electrophysiologyACTA OPHTHALMOLOGICA, Issue 2010GE HOLDER Purpose To describe the roles of electrophysiology in patients with medically unexplained visual loss Methods Standardised full-field and pattern ERGs and VEPs; additional pattern appearance VEPs to quantify visual system resolution when necessary in patients with suspected non-organic visual loss. Results Selected cases will be used to illustrate the roles of electrophysiology. A diagnosis of non-organic visual loss is confirmed by the demonstration of normal visual system function in the presence of symptoms that suggest otherwise. Patients with optic nerve disease may have a normal fundus appearance, and not all macular dysfunction is associated with an abnormal appearance of the macula; both pattern VEP and pattern ERG are needed in such cases. Further, there are many patients with retinal disease where the fundus appearance may be normal but ERGs are abnormal. Conclusion Objective functional assessment with electrophysiology is indispensable to the diagnosis and management of patients with medically unexplained visual loss. [source] 4412: Immunohistochemistry and Western blot methodologies to evaluate neuroprotective agents in models of retinopathiesACTA OPHTHALMOLOGICA, Issue 2010K THERMOS Purpose Many retinopathies that lead to visual loss and blindness are characterized by neovascularization and neural retinal defects, such as a marked loss in retinal neurons and an increase in apoptosis. There are no therapeutic agents for the treatment of the neurodegenerative component of retinal disease. Immunohistochemistry and western blot methodologies were employed to determine retinal viability and to elucidate the putative neuroprotective properties of new therapeutic targets, in animal models of retinopathy (chemical ischemia, excitotoxicity, STZ). Methods To assay retinal viability, the following antibodies for retinal markers were employed in immunohistochemical assays: PKC (rod bipolar cells), ChAT, bNOS, TH (cholinergic-, nitric oxide synthetase-, and dopamine- containing amacrine cells, respectively), calbindin-containing horizontal, amacrine and cone bipolar cells, NFL and MAP1 (ganglion axons and cells, respectively). Antibodies against various pro-survival or pro-death molecules (western blots), as well as the TUNEL-assay, were employed to examine retinal apoptosis and neuroprotection. Results Loss of retinal marker immunoreactivity was differentially observed according to the animal model employed. The neuroprotection of specific retinal neurons by the new therapeutic targets examined (somatostatin and neurosteroids) reflect the existence of protein substrates involved in the mechanism of action of these molecules. Conclusion Immunohistochemical and western blot analysis techniques provide important information on the retinal damage induced by ischemic insults and the neuroprotection afforded by new targets of retinal therapeutics. [source] 3162: Traumatic chiasmal and retrochiasmal dysfunctionACTA OPHTHALMOLOGICA, Issue 2010FX BORRUAT Chiasmal or retrochiasmal dysfunction can result from head trauma. Usually it is associated with a violent trauma such as car accident or fall from several meters. Their incidence is low but may be underdiagnosed. The frequency, the mechanisms, and the clinical presentations of such traumatic visual loss will be reviewed in this presentation. [source] 3331: The genetics of corneal dystrophiesACTA OPHTHALMOLOGICA, Issue 2010GCM BLACK Purpose To provide an overview of progress in understanding of the genetics of corneal dystrophies. Methods A systematic review, including case presentations, to illustrate insights into genes underlying inherited corneal dystrophies: Results Recent advances have extended our undestanding of the causation of a range of classical inherited corneal dystrophies. This includes the identifcation of genes underlying superficial (e.g Meesmann, KRT3/KRT12), stromal (BIGH3/TGFB1) and endothelial (SLC4A11, COL8A2) dysrophies. Understanding of less well-recognised phenotypes (e.g brittle cornea syndrome) has also shed light on the regulation of corneal homeostasis including the control of corneal thickness. Conclusion Identification of the genes underlying corneal inherited disease improves diagnosis of corneal dysrophies, sheds light on disease mechanisms and has potential to improve patient management. In the futuire this will lead to new therapeutic modalities for an important group of conditions associated with significant visual loss. [source] | ||||||||||