Search

BACKGROUND: Tetrachloroethylene (PCE; or perchloroethylene) has been implicated in visual impairments among adults with occupational and environmental exposures as well as children born to women with occupational exposure during pregnancy. [...]

Retinal and choroidal vascular diseases, with their associated abnormalities in vascular permeability, account for the majority of patients with vision loss in industrialized nations. VEGF is upregulated in ischemic retinopathies such as diabetes and is known to dramatically alter vascular permeability in a number of nonocular tissues via Src kinase--regulated signaling pathways. VEGF antagonists are currently in clinical use for treating the new blood vessels and retinal edema associated with neovascular eye diseases, but such therapies require repeated intraocular injections. We have found that vascular leakage following intravitreal administration of VEGF in mice was abolished by systemic or topical delivery of what we believe is a novel VEGFR2/Src kinase inhibitor; this was confirmed in rabbits. The relevance of Src inhibition to VEGF-associated alterations in vascular permeability was further substantiated by genetic studies in which VEGF injection or laser-induced vascular permeability failed to augment retinal vascular permeability in Src-/- and Yes-/- mice (Src and Yes are ubiquitously expressed Src kinase family members; Src-/- and Yes-/- mice lacking expression of these kinases show no vascular leak in response to VEGF). These findings establish a role for Src kinase in VEGF-mediated retinal vascular permeability and establish a potentially safe and painless topically applied therapeutic option for treating vision loss due to neovascular-associated retinal edema., Introduction Abnormal retinal vascular permeability leading to edema in the area of the macula is the leading cause of vision loss in diseases such as diabetic retinopathy, exudative macular degeneration, [...]

Neuroprotection can be achieved by preventing apoptotic death of postmitotic cells. Apoptotic death can occur by either a caspase-dependent mechanism, involving cytochrome c, apoptosis protease-activating factor-1 (Apaf-1), and caspase-9, or a caspase-independent mechanism, involving apoptosis-inducing factor (AIF). HIV protease inhibitors (PIs) avert apoptosis in part by preventing mitochondrial outer membrane permeabilization (MOMP), but the precise mechanism by which they work is not known. Here, we evaluated the impact of the PIs in a mouse model of retinal detachment (RD) in vivo and in murine primary retinal cell cultures in vitro. Oral administration of the PIs nelfinavir and ritonavir significantly inhibited photoreceptor apoptosis, while preventing the translocation of AIF from mitochondria to the nucleus as well as the activation of caspase-9. RD-induced photoreceptor apoptosis was similarly inhibited in mice carrying hypomorphic mutations of the genes encoding AIF or Apaf-1. Nelfinavir attenuated apoptosis as well as mitochondrial release of AIF and cytochrome c, and subsequent activation of caspase-9 in vitro, in photoreceptor cultures exposed to starvation or monocyte chemoattractant protein-1-stimulated (MCP-1-stimulated) macrophages. Our results suggest that the MOMP inhibition by PIs involved interruption of both caspase-dependent and caspase-independent apoptosis pathways and that PIs may be clinically useful for the treatment of diseases caused by excessive apoptosis., Introduction Photoreceptor apoptosis after retinal detachment (RD) is a major cause of permanent visual loss in various diseases. Detachment of the retina from underlying retinal pigment epithelium (RPE) occurs in [...]

Elevated intraocular pressure (IOP) is the principal risk factor for glaucoma and results from excessive impedance of the fluid outflow from the eye. This abnormality likely originates from outflow pathway tissues such as the trabecular meshwork (TM), but the associated molecular etiology is poorly understood. We discovered what we believe to be a novel role for secreted frizzled-related protein-1 (sFRP-1), an antagonist of Wnt signaling, in regulating IOP. sFRP1 was overexpressed in human glaucomatous TM cells. Genes involved in the Wnt signaling pathway were expressed in cultured TM cells and human TM tissues. Addition of recombinant sFRP-1 to ex vivo perfusion-cultured human eyes decreased outflow facility, concomitant with reduced levels of [beta]-catenin, the Wnt signaling mediator, in the TM. Intravitreal injection of an adenoviral vector encoding sFRP1 in mice produced a titer-dependent increase in IOP. Five days after vector injection, IOP increased 2 fold, which was significantly reduced by topical ocular administration of an inhibitor of a downstream suppressor of Wnt signaling. Thus, these data indicate that increased expression of sFRP1 in the TM appears to be responsible for elevated IOP in glaucoma and restoring Wnt signaling in the TM may be a novel disease intervention strategy for treating glaucoma., Introduction Glaucoma is a major cause of irreversible visual impairment and blindness in the world (1), (2). Approximately 70 million individuals have this disease, although more than half of the [...]

Many patients will experience some type of visual dysfunction following a stroke. The visual changes associated with stroke can be categorized as sensory (visual acuity and visual field), motor (extraocular [...]

The retina is among the most metabolically active tissues in the body, requiring a constant supply of blood glucose to sustain function. We assessed the impact of low blood glucose on the vision of C57BL/6J mice rendered hypoglycemic by a null mutation of the glucagon receptor gene, Gcgr. Metabolic stress from moderate hypoglycemia led to late-onset loss of retinal function in [Gcgr.sup.-/-] mice, loss of visual acuity, and eventual death of retinal cells. Retinal function measured by the electroretinogram b-wave threshold declined >100-fold from age 9 to 13 months, whereas decreases in photoreceptor function measured by the ERG a-wave were delayed by 3 months. At 10 months of age [Gcgr.sup.-/-] mice began to lose visual acuity and exhibit changes in retinal anatomy, including an increase in cell death that was initially more pronounced in the inner retina. Decreases in retinal function and visual acuity correlated directly with the degree of hypoglycemia. This work demonstrates a metabolic-stress-induced loss of vision in mammals, which has not been described previously. Linkage between low blood glucose and loss of vision in mice may highlight the importance for glycemic control in diabetics and retinal diseases related to metabolic stress as macular degeneration. C57BL/6J mice | cell death | glucagon receptor gene | retinal function | visual acuity

A study to estimate the number of US individuals aged 12 years or older who have impaired distance vision due to uncorrected refractive error is presented. The results suggest that approximately 14 million individuals aged 12 years or older were estimated to be visually impaired and more than 11 million of these individuals could attain visual acuity good enough to qualify them for a driver's license in most states with refractive correction.

We report 13 cases of ophthalmic complications resulting from dengue infection in Singapore. We performed a retrospective analysis of a series of 13 patients with dengue fever who had visual [...]

Vision loss caused by ocular neovascularization in diabetic retinopathy and exudative age-related macular degeneration (ARMD) can be prevented by using molecular medicines. Details about various researches carried out in the angiogenesis and discussions regarding vascular endothelial growth factor are discussed.

This paper presents estimates of the prevalence of visual impairment and its causes in 2002, based on the best available evidence derived from recent studies. Estimates were determined from data on low vision and blindness as defined in the International statistical classification of diseases, injuries and causes of death, 10th revision. The number of people with visual impairment worldwide in 2002 was in excess of 161 million, of whom about 37 million were blind. The burden of visual impairment is not distributed uniformly throughout the world: the least developed regions carry the largest share. Visual impairment is also unequally distributed across age groups, being largely confined to adults 50 years of age and older. A distribution imbalance is also found with regard to gender throughout the world: females have a significantly higher risk of having visual impairment than males. Notwithstanding the progress in surgical intervention that has been made in many countries over the last few decades, cataract remains the leading cause of visual impairment in all regions of the world, except in the most developed countries. Other major causes of visual impairment are, in order of importance, glaucoma, age-related macular degeneration, diabetic retinopathy and trachoma. Keywords Vision, Low/epidemiology; Blindness/epidemiology; Vision, Low/etiology; Blindness/etiology; Cataract/complications; Glaucoma/complications; Macular degeneration/complications; Refractive errors/complications; Cost of illness; Age factors; Sex factors (source: MESH, NLIVl). Mots cles Baisse vision/epidemiologie; Cecite/epidemiologie; Baisse vision/etiologie; Cecite/etiologie; Cataracte/complication; Glaucome/complication; Degenerescence maculaire/complication; Troubles refraction oculaire/complication; Cout maladie; Facteur age; Facteur sexuel (source: MeSH, INSERM). Palabras clave Vision subnormal/epidemiologia; Ceguera/epidemiologia; Vision subnormal/etiologia; Ceguera/etiologia; Catarata/ complicaciones; Glaucoma/complicaciones; Degeneracion macular/complicaciones; Errores de refraccion/complicaciones; Costo de la enfermedad; Factores de edad; Factores sexuales (fuente: DeCS, BIREME). [TEXT NOT REPRODUCIBLE IN ASCII], Resume Donnees mondiales sur les deficiences visuelles pour l'annee 2002 Le present article estime la prevalence des deficiences visuelles et de leurs causes en 2002 a partir des meilleures donnees [...]

Ocular trauma or disease may lead to severe corneal opacification and consequently severe loss of vision as a result of complete loss of corneal epithelial stem cells. Sutureless transplantation of carrier-free cell sheets composed of autologous oral mucosal epithelial cells could be used to reconstruct corneal surfaces and restore vision in patients with bilateral severe disorders of the ocular surface.

Byline: Adolfo M. Bronstein (1) Keywords: vertigo; vestibular disorders; oscillopsia; vision Abstract: Abstract. This review deals with two syndromes, oscillopsia and visual vertigo. Oscillopsia is the illusion of oscillation of the visual surroundings. For diagnosis purposes one should ask, when does the oscillopsia occur? If oscillopsia is only present during head (or whole body) movements, the likely underlying cause is a bilateral defect in the vestibulo-ocular reflex (VOR). The more common causes are post meningitic vestibular damage, gentamicin ototoxicity or bilateral idiopathic vestibular failure. When oscillopsia develops after specific head positions, it is usually due to a positional nystagmus, usually the result of brainstem-cerebellar disease. When the oscillopsia is largely unrelated to head movements, one should ask, is it fairly constant or is it in attacks (paroxysmal)? If the oscillopsia is constant it is usually due to the presence of a clinically observable nystagmus the most common is downbeat nystagmus but the most visually disabling is pendular nystagmus. If the oscillopsia comes in brief attacks it is usually due to a paroxysmal nystagmus as observed in irritative VIII nerve and brainstem lesions. However, the most common cause of paroxysmal oscillopsia is a non organic condition called voluntary nystagmus. Treatment of oscillopsia is often pharmacological but disappointing the best chance of success is carbamazepine for paroxysmal disorders secondary to structural vestibular nerve/nuclear lesions. Visual vertigo should not be confused with oscillopsia. It can be defined as dizziness provoked by visual environments with large size (full field) repetitive or moving visual patterns. Patients with visual vertigo report discomfort in supermarkets and when viewing movement of large visual objects, eg crowds, traffic, clouds or foliage. Visual vertigo is present in many patients with a history of a peripheral vestibular disorder, particularly those who are visually dependent (ie subjects who use vision preferentially for postural and space orientation control). Patients with visual vertigo benefit from the addition to their standard vestibular rehabilitation of optic flow (optokinetic) stimuli and exercises involving visuo-vestibular conflict. Author Affiliation: (1) Academic Department of Neuro-Otology, Division of Neuroscience and Psychological Medicine, Imperial College London, Charing Cross Hospital, London W6 8RF, UK Article History: Registration Date: 01/01/2004 Received Date: 16/01/2004 Accepted Date: 21/01/2004

Byline: Ulrich Schiefer (1) Author Affiliation: (1) Dept. of Pathophysiology of Vision and Neuro-Ophthalmology, University Eye Hospital Tuebingen, Schleichstr. 12--16, 72076 Tubingen, Germany. ulrich.schiefer@uni-tuebingen.de, DE Article note: Received: 18 January 2003, Accepted: 30 January 2003 Correspondence to Prof. Dr. med. Ulrich Schiefer

Byline: Selcuk Comoglu (1), Alper Yarangumeli (2), Ozlem Gurbuz Koz (2), Atilla Halil Elhan (3), Gulcan Kural (2) Keywords: Key words migraine; visual field; normal tension glaucoma Abstract: Purpose: To investigate the visual fields in patients with migraine in terms of glaucomatous visual field defects. Method: Patients who attended our Neurology outpatient clinic complaining of headache and were diagnosed as migraine were enrolled in the study. Each patient was questioned for the frequency, side, localisation and severeness of the pain as well as the onset and the duration of the symptoms, the existence of aura, the description of the aura -- if present --, additional systemic problems, and family history of migraine and glaucoma. Detailed ophthalmological examinations and computerised visual field (VF) analysis were then performed on each patient in our Ophthalmology Clinic. The findings of 77 patients (61 female, 16 male) were evaluated and statistical comparisons were carried out between the group of patients with glaucomatous-like VF defects and the group without significant defects. Results: VF tests revealed glaucomatous-like defects in 48 (62.3 %) patients. Intraocular pressure (IOP) levels were within normal limits in all cases. There were no statistically significant differences between the groups with and without VF defects in terms of sex, the localisation and severeness of pain, the existence and the description of aura, and family history of glaucoma, as well as the duration of migraine, IOP and cup/disc ratio. The glaucomatous group was significantly older, with a significantly higher age of onset for migraine. Risk of having glaucomatous-like defects was higher in patients who had migraine attacks once a month or less frequently. A tendency of pain and VF defects to develop ipsilaterally was noticed. Discussion: A possible relationship between the pathophysiology of migraine, visual field defects and glaucomatous optic neuropathy is emphasized and VF screening for normal tension glaucoma is recommended in patients with migraine. Author Affiliation: (1) from Ankara Numune Training and Research Hospital, Neurology Clinic, Ankara, Turkey, TR (2) from Ankara Numune Training and Research Hospital, 1st Eye Clinic, Ankara, Turkey, TR (3) from Medical Faculty of Ankara University, Division of Biostatistics, Ankara, Turkey, TR (4) Guvenlik Cad. 22/15, A.AyrancA+- 06540, Ankara, Turkey. alperyx@yahoo.com, TR Article note: Received: 4 February 2002, Received in revised form: 10 September 2002, Accepted: 16 September 2002 Correspondence to Alper Yarangumeli

Byline: Jan Lycke (1), Per Olof Tollesson (3), Lars Frisen (2) Keywords: Key words Multiple sclerosis; Optic neuritis; Resolution perimetry; Vision Abstract: Visual disturbances are common in multiple sclerosis (MS) and often a result of acute demyelinating optic neuropathy. Careful examination of MS patients, who have never suffered optic neuritis, may also reveal asymptomatic visual loss. This type of silent disease activity was investigated by computerised resolution perimetry, which has the potential to reflect the percentage of functional retino-cortical neural channels. The time of onset and the evolution of asymptomatic visual loss was investigated. One approach was to retrospectively select patients who never had suffered acute optic neuritis from a closely monitored MS population and re-examine them again. Sixteen patients were identified and vision was evaluated during a period of 5.5--9 years of follow-up and compared with that in 14 healthy controls. The mean channel percentage of the MS group was 89 +- 19 % (SD) on entry into the study, compared with 110 +- 15 % (SD) of controls (p &lt 0.003). At termination of the study the mean percentage was essentially unchanged both in MS patients (87 +- 21 %, SD) and controls (110 +- 19 %, SD). The second approach was to test a group of 7 patients with MS or strongly suspected MS, with the same method, in close connection with their first clinical exacerbation. All cases lacked visual symptoms and none had previously had acute visual loss. Again, virtually all performed subnormally in the vision tests, and to the same degree as in the first group of patients. Results were compared with those obtained from 25 MS patients who had experienced one or more attacks of optic neuritis. Compared with controls the loss of functional retino-cortical neural channels was 20 % in patients without a previous history of optic neuritis and 30 % in patients who previously had experienced optic neuritis. We conclude that asymptomatic visual loss seems to be a universal feature of MS and has a substantial impact on the visual pathways, that it is present already at the time of clinical onset of the disease, and that any progression thereafter is slow enough to elude detection during several years of follow-up. Author Affiliation: (1) Institute of Clinical Neuroscience, Department of Neurology, Goteborg University, Sahlgren's University Hospital, 41345 Goteborg, Sweden, Tel.: +46-31/3 42 32 10, Fax: +46-31/82 62 27, E-Mail: jan.lycke@neuro.gu.se, SE (2) Institute of Clinical Neuroscience, Dep. of Ophthalmology, Goteborg University, SE (3) Institute of Radiology, Department of Neuroradiology, Goteborg University, SE Article note: Received: 28 June 2000, Received in revised form: 7 March 2001, Accepted: 23 April 2001