A Study of Surgical Approaches to Retinal Vascular Occlusions
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Imaging Options in Retinal Vein Occlusion Management of This Condition Should Take Direction from Clinical Trial Results
Imaging Options in Retinal Vein Occlusion Management of this condition should take direction from clinical trial results. BY NIDHI RELHAN, MD; WILLIAM E. SMIDDY, MD; AND DELIA CABRERA DEBUC, PHD etinal vein occlusion (RVO) is the Objectively assessing RVO severity Laser Photocoagulation second leading cause of retinal and determining prognosis of the The Branch Vein Occlusion Study vascular disease, with reported condition depend on imaging stud- (BVOS) recommended focal laser pho- cumulative annual incidence of ies. All clinical trials in RVO have tocoagulation for BRVO causing visual 1.8% for branch RVO (BRVO) and relied heavily on various imaging acuity of 20/40 or worse and macular R0.5% for central RVO (CRVO),1,2 and modalities to standardize eligibil- edema.13,14 Evidence of center-involving bilateral or subsequent incidences of ity and treatment monitoring. This macular edema on fluorescein angiogra- 6.4% and 0.9%, respectively.1,3,4 article reviews the use of some phy (FA) was the critical entry criterion. The postulated mechanism of action established imaging modalities in Separately, scatter photocoagulation involves impingement of venules at these important clinical trials and to the involved segment was found to the shared adventitial sheath by cross- looks ahead at some promising new prevent occurrence of vitreous hemor- ing arterioles leading to turbulence, imaging technologies. rhage if neovascularization developed. stasis, thrombosis, and occlusion.5,6 The Central Vein Occlusion Study Response to anti-VEGF and antiinflam- ESTABLISHED TREATMENT OPTIONS (CVOS) reported that panretinal matory agents has empirically dem- Management of RVO with laser photocoagulation reduced visual onstrated that inflammatory factors photocoagulation, anti-VEGF agents, loss when 2 or more clock hours of play a more important role in RVO and corticosteroids has been well iris neovascularization or more than than previously presumed, beyond established (Tables 1 and 2).13-29 10 disc areas of capillary nonperfusion the obvious ischemia. -
Fundus Signs in Temporal Arteritis
Br J Ophthalmol: first published as 10.1136/bjo.62.9.591 on 1 September 1978. Downloaded from British Journal of Ophthalmology, 1978, 62, 591-594 Fundus signs in temporal arteritis D. McLEOD, E. 0. OJI, E. M. KOHNER, AND J. MARSHALL From Moorfields Eye Hospital and Institute of Ophthalmology, London SUMMARY A patient with temporal arteritis developed a variety of ischaemic lesions in the eyes. Infarction of the inner retina and optic nerve head was delineated on presentation by white swelling in the retinal nerve fibre layer. The role of interrupted axoplasmic transport in the production of this sign is discussed. Outer retinal infarction was also noted on presentation and subsequently gave rise to striking pigmented scars. Temporal arteritis often presents with visual loss, the central venous tributaries were of normal and necropsy examination in such cases shows wide- calibre and colour. No abnormality of the inner spread disease of the ophthalmic artery and the retina was noted in the territory of supply of the extraocular course of its ciliary and retinal branches central retinal artery. (Henkind et al., 1970). The medial and lateral At first sight the left eye showed a similar ophthal- posterior ciliary arteries supply the optic nerve head, moscopic picture, with pale swelling of the nasal the outer retina, and, in 20 to 50% of individuals, part of the optic disc and a row of fluffy white by copyright. a variable area of inner retina contiguous with the cotton-wool spots crossing the papillomacular optic disc (Hayreh, 1969); the central retinal artery bundle (Fig. 2). -
Microsurgical Anatomy of the Central Retinal Artery
Original Article Microsurgical Anatomy of the Central Retinal Artery Matias Baldoncini1,2, Alvaro Campero2,3, Gabriel Moran1, Maximiliano Avendan˜ o1, Pablo Hinojosa-Martı´nez1, Marcela Cimmino1, Pablo Buosi1, Valeria Forlizzi1, Joaquı´n Chuang1, Brian Gargurevich1 - BACKGROUND: The central retinal artery (CRA) has INTRODUCTION been described as one of the first branches of the he central retinal artery (CRA) is described as one of the ophthalmic artery.It arises medial to the ciliary ganglion first branches of the ophthalmic artery. It arises medial to and after a sinuous path within the orbital cavity it pene- T the ciliary ganglion, and after a sinuous path inside the trates the lower surface of the dura mater that covers the orbital cavity, penetrates the lower surface of the dura mater that optic nerve, approximately 1 cm behind the eyeball. How- covers the optic nerve, approximately 1 cm behind the eyeball. ever, the numerous anatomic descriptions that were made After a short journey inside this meninge, it crosses the cranial of the CRA have been insufficient or unclear in relation to nerve to be located in its center and travels until it reaches the optical papilla where it divides into several branches. During this certain characteristics that are analyzed in the present entire journey, the CRA does not present any anastomoses, study. considering it as a terminal branch.1-4 However, the descriptions that many investigators make about - METHODS: An electronic literature search was made in some of thesecharacteristics of the CRA differ with the classic the PubMed database and a cadaver dissection was per- disposition] (Tables 1e12).5-40 The numerous anatomic de- formed on 11 orbits fixed in formaldehyde. -
THE CENTRAL ARTERY of the RETINA*T H
Br J Ophthalmol: first published as 10.1136/bjo.44.5.280 on 1 May 1960. Downloaded from Brit. J. Ophthal. (1960) 44, 280. THE CENTRAL ARTERY OF THE RETINA*t H. A STUDY OF ITS DISTRIBUHTION AND ANASTOMOSES BY SOHAN SINGH AND RAMJI DASS Department ofAnatomy, Government Medical College, Patiala, India THERE is little unanimity regarding the distribution and anastomoses of the central artery of the retina. According to Frangois and Neetens (1954, 1956) and Fran9ois, Neetens, and Collette (1955), the central artery of the retina is completely devoid of branches, while according to Wolff (1939) and Behr (1935) it is free from branches only in its intraneural course. Magitot (1908), Quain (1909), Beauvieux and Ristitch (1924), Wolff (1940), Bignell (1952), Wybar (1956), and Steele and Blunt (1956) on the other hand demon- strated branches from all parts of its course. Most investigators agree that this artery contributes to the blood supply of the optic nerve, but Francois and others (1954, 1955, 1956) affirm that this is not the case. The presence of a central artery of the optic nerve described by Behr (1935), Wolff (1939, 1954), Francois and others (1954, 1955, 1956), and Wybar (1956), is denied by Beauvieux and Ristitch (1924) and Steele and Blunt (1956). Beauvieux and Ristitch (1924), Kershner (1943), Frangois and others http://bjo.bmj.com/ (1954, 1955, 1956), and Steele and Blunt (1956) say there are no anastomoses between the central retinal and other arteries, but Vail (1948), Wybar (1956), and several other authors have observed and described them. The lamina cribrosa is the only site at which these anastomoses have been studied in any detail, and in this case too, contradictory views have been expressed. -
Ultrasound Enhanced Thrombolysis in Experimental Retinal Vein Occlusion in the Rabbit
1438 Br J Ophthalmol 1998;82:1438–1440 Ultrasound enhanced thrombolysis in experimental retinal vein occlusion in the rabbit Jörgen Larsson, Jonas Carlson, S Bertil Olsson Abstract such as myocardial infarction, which is life Aims—To investigate if it was possible to threatening, this incidence of haemorrhage is lower the dose of streptokinase and main- acceptable, but in a patient with a retinal vein tain an eVective thrombolysis by adding occlusion it is hard to accept life threatening pulsed low energy ultrasound. side eVects. Methods—53 retinal veins in 27 rabbits Dye enhanced photothrombosis is a method were occluded by rose bengal enhanced where a dye that absorbs maximally at a laser treatment. Six rabbits were treated specific wavelength is injected intravenously with streptokinase (50 000 IU/kg), 10 rab- immediately before laser treatment in order to bits were treated with a low dose of strep- enhance the absorption of the laser light and tokinase (25 000 IU/kg), and 11 rabbits thus making it possible to use less laser energy. were treated with a low dose of streptoki- This method easily produces thrombi in the nase (25 000 IU/kg) and pulsed ultrasound vessels.18–20 during 1 hour. Fluorescein angiography Based on earlier in vitro experiences21 22 we was performed immediately before the wanted to investigate whether it was possible to thrombolytic treatment and after 12 lower the dose of streptokinase by adding hours. pulsed low energy ultrasound towards a Results—In the group treated with strep- thrombus in the eye. We investigated this in a tokinase (50 000 IU/kg) all vessels were model of experimental retinal vein occlusion in open. -
The Bowman Lecture Papilloedema
THE BOWMAN LECTURE PAPILLOEDEMA: 'THE PENDULUM OF PROGRESS' M. D. SANDERS London I. HISTORICAL BACKGROUND appreCiatIOn a gift in the form of a compound One year after the Battle of Waterloo, William microscope. This may have been one of the crucial Bowman was born into a world entering a period of events in his life, for though the compound micro dramatic change. The new age of science would see scope was developed in the previous century, the transport and communication revolutionised and the chromatic aberration was only overcome in 1830 by purpose of human existence shaken by Darwin's Lord Lister's father, just before the gift was made to thoughts on natural selection. Surgery would benefit Bowman. from the techniques of antisepsis and the first Thus in 1837 Queen Victoria ascended the throne, anaesthetic would be administered. In ophthalmol and William Bowman aged 21 entered the portals of King's College in London's Strand fully equipped to ogy the description of glaucoma and the invention of contribute to the explosion in knowledge that was the ophthalmoscope would enable the specialty to about to erupt. Todd, the new Professor of Physiol survive in its own right, with the inception of its own ogy at King's, was using his phenomenal enthusiasm society. to compile two massive books on the anatomy and Bowman's introduction to medicine probably physiology of the whole body. resulted from an initial injury inflicted to his ha.nd Bowman described the voluntary and involuntary whilst experimenting with gunpowder as a boy.1 He muscles4 and their actions without formal methods of consulted the Birmingham Surgeon Joseph Hodgson fixing or staining specimens, and no microtome. -
Reverberating Flow Pattern in the Central Retinal Artery in Cerebral
NEUROIMAGES Reverberating flow pattern in the central retinal artery in cerebral circulatory arrest Pablo Blanco, MD, Mar´ıa Fernanda Men´endez, MD, and Liliana Figueroa, MD Correspondence Dr. Blanco Neurology 2020;94:276-277. doi:10.1212/WNL.0000000000008918 ® [email protected] Figure 1 Transcranial Doppler and central retinal arteries (CRA) waveforms (A) Reverberating flow pattern in the right (and left, not shown) middle cerebral artery (MCA). (B) The right (and left, not shown) CRA showed similar waveforms to MCA. Figure 2 Technique for ultrasound assessment of the central retinal arteries (CRA) flow (A) A linear transducer is placed in an axial position over the globe, with the eyelids closed and covered by a generous amount of gel. (B) In color Doppler, the CRA (a) is coded red, indicating flow moving toward the globe (G), while the central retinal vein (v) is coded blue, indicating flow moving away from the globe. (C) In spectral Doppler, the CRA typically shows low resistance velocity waveforms (represented in the anterograde channel), while the central retinal vein has a phasic flow (represented in the retrograde channel). From the “Centro Unico´ Coordinador de Ablacion´ e Implante Provincia de Buenos Aires (CUCAIBA)” Team, “Dr. Emilio Ferreyra” Hospital, Necochea, Argentina. Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article. 276 Copyright © 2020 American Academy of Neurology Copyright © 2020 American Academy of Neurology. Unauthorized reproduction of this article is prohibited. A 49-year-old woman developed signs of brain death after when obtaining flow signals through the cranial bone is not a severe traumatic brain injury. -
The Ophthalmic Artery Ii
Brit. J. Ophthal. (1962) 46, 165. THE OPHTHALMIC ARTERY II. INTRA-ORBITAL COURSE* BY SOHAN SINGH HAYREHt AND RAMJI DASS Government Medical College, Patiala, India Material THIS study was carried out in 61 human orbits obtained from 38 dissection- room cadavers. In 23 cadavers both the orbits were examined, and in the remaining fifteen only one side was studied. With the exception of three cadavers of children aged 4, 11, and 12 years, the specimens were from old persons. Method Neoprene latex was injected in situ, either through the internal carotid artery or through the most proximal part of the ophthalmic artery, after opening the skull and removing the brain. The artery was first irrigated with water. After injection the part was covered with cotton wool soaked in 10 per cent. formalin for from 24 to 48 hours to coagulate the latex. The roof of the orbit was then opened and the ophthalmic artery was carefully studied within the orbit. Observations COURSE For descriptive purposes the intra-orbital course of the ophthalmic artery has been divided into three parts (Singh and Dass, 1960). (1) The first part extends from the point of entrance of the ophthalmic artery into the orbit to the point where the artery bends to become the second part. This part usually runs along the infero-lateral aspect of the optic nerve. (2) The second part crosses over or under the optic nerve running in a medial direction from the infero-lateral to the supero-medial aspect of the nerve. (3) The thirdpart extends from the point at which the second part bends at the supero-medial aspect of the optic nerve to its termination. -
Diagnosis and Management of Central Retinal Vein Occlusion
RETINA OPHTHALMIC PEARLS Diagnosis and Management of Central Retinal Vein Occlusion etinal vein occlusion (RVO) has Ocular conditions. Open-angle glau- 1 a prevalence of 0.5%, making coma is a major ocular risk factor for Rit the second most-common CRVO. retinal vascular disorder after diabetic In addition, individuals with CRVO retinopathy.1 RVO is classified accord- in 1 eye are at higher risk of developing ing to the anatomic level of the occlu- CRVO in the fellow eye.2 In the Central sion, with 3 major distinct entities: Vein Occlusion Study (CVOS), 4% of • Central retinal vein occlusion patients presented with bilateral CRVO (CRVO): occlusion of the central reti- at study enrollment, and a further 5% nal vein at the level of, or posterior to, had evidence of previous CRVO in the the lamina cribrosa (Fig. 1) fellow eye at baseline. In the remaining • Hemiretinal vein occlusion (HRVO): subjects, 1.4% developed CRVO in the occlusion at the disc, involving either fellow eye during 3 years of follow-up. ACUTE CRVO. Classic “blood and thun- the superior or inferior hemiretina Other ocular risk factors include der” fundus appearance of a patient • Branch retinal vein occlusion retrobulbar external compression of the presenting acutely with central retinal (BRVO): occlusion of a tributary vein, central retinal vein, as occurs in thyroid vein occlusion of the right eye. typically at the site of an arteriovenous orbitopathy, or compression by intra- crossing; thought to be caused by com- orbital space-occupying lesions. may be absent. In subacute or late pression from an overlying atheroscle- presentations in which disc swelling rotic arteriole Clinical Presentation has resolved (with or without collateral This article will focus on diagnosis Patients with CRVO typically present vessel formation), the flame-shaped and management of the first entity, with a history of unilateral acute, pain- hemorrhages clear first, leaving deeper CRVO. -
Anatomy and Physiology of the Afferent Visual System
Handbook of Clinical Neurology, Vol. 102 (3rd series) Neuro-ophthalmology C. Kennard and R.J. Leigh, Editors # 2011 Elsevier B.V. All rights reserved Chapter 1 Anatomy and physiology of the afferent visual system SASHANK PRASAD 1* AND STEVEN L. GALETTA 2 1Division of Neuro-ophthalmology, Department of Neurology, Brigham and Womens Hospital, Harvard Medical School, Boston, MA, USA 2Neuro-ophthalmology Division, Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, PA, USA INTRODUCTION light without distortion (Maurice, 1970). The tear–air interface and cornea contribute more to the focusing Visual processing poses an enormous computational of light than the lens does; unlike the lens, however, the challenge for the brain, which has evolved highly focusing power of the cornea is fixed. The ciliary mus- organized and efficient neural systems to meet these cles dynamically adjust the shape of the lens in order demands. In primates, approximately 55% of the cortex to focus light optimally from varying distances upon is specialized for visual processing (compared to 3% for the retina (accommodation). The total amount of light auditory processing and 11% for somatosensory pro- reaching the retina is controlled by regulation of the cessing) (Felleman and Van Essen, 1991). Over the past pupil aperture. Ultimately, the visual image becomes several decades there has been an explosion in scientific projected upside-down and backwards on to the retina understanding of these complex pathways and net- (Fishman, 1973). works. Detailed knowledge of the anatomy of the visual The majority of the blood supply to structures of the system, in combination with skilled examination, allows eye arrives via the ophthalmic artery, which is the first precise localization of neuropathological processes. -
A Review of Central Retinal Artery Occlusion: Clinical Presentation And
Eye (2013) 27, 688–697 & 2013 Macmillan Publishers Limited All rights reserved 0950-222X/13 www.nature.com/eye 1 2 1 2 REVIEW A review of central DD Varma , S Cugati , AW Lee and CS Chen retinal artery occlusion: clinical presentation and management Abstract Central retinal artery occlusion (CRAO) is an that in turn place an individual at risk of future ophthalmic emergency and the ocular ana- cerebral stroke and ischaemic heart disease. logue of cerebral stroke. Best evidence reflects Although analogous to a cerebral stroke, there that over three-quarters of patients suffer is currently no guideline-endorsed evidence for profound acute visual loss with a visual acuity treatment. Current options for therapy include of 20/400 or worse. This results in a reduced the so-called ‘standard’ therapies, such as functional capacity and quality of life. There is sublingual isosorbide dinitrate, systemic also an increased risk of subsequent cerebral pentoxifylline or inhalation of a carbogen, stroke and ischaemic heart disease. There are hyperbaric oxygen, ocular massage, globe no current guideline-endorsed therapies, compression, intravenous acetazolamide and although the use of tissue plasminogen acti- mannitol, anterior chamber paracentesis, and vator (tPA) has been investigated in two methylprednisolone. None of these therapies randomized controlled trials. This review will has been shown to be better than placebo.5 describe the pathophysiology, epidemiology, There has been recent interest in the use of and clinical features of CRAO, and discuss tissue plasminogen activator (tPA) with two current and future treatments, including the recent randomized controlled trials on the 1Flinders Comprehensive use of tPA in further clinical trials. -
Anatomy of the Ophthalmic Artery: Embryological Consideration
REVIEW ARTICLE doi: 10.2176/nmc.ra.2015-0324 Neurol Med Chir (Tokyo) 56, 585–591, 2016 Online June 8, 2016 Anatomy of the Ophthalmic Artery: Embryological Consideration Naoki TOMA1 1Department of Neurosurgery, Mie University Graduate School of Medicine, Tsu, Mie, Japan Abstract There are considerable variations in the anatomy of the human ophthalmic artery (OphA), such as anom- alous origins of the OphA and anastomoses between the OphA and the adjacent arteries. These anatomi- cal variations seem to attribute to complex embryology of the OphA. In human embryos and fetuses, primitive dorsal and ventral ophthalmic arteries (PDOphA and PVOphA) form the ocular branches, and the supraorbital division of the stapedial artery forms the orbital branches of the OphA, and then numerous anastomoses between the internal carotid artery (ICA) and the external carotid artery (ECA) systems emerge in connection with the OphA. These developmental processes can produce anatomical variations of the OphA, and we should notice these variations for neurosurgical and neurointerventional procedures. Key words: ophthalmic artery, anatomy, embryology, stapedial artery, primitive maxillary artery Introduction is to elucidate the anatomical variation of the OphA from the embryological viewpoint. The ophthalmic artery (OphA) consists of ocular and orbital branches. The ocular branches contribute to Embryology and Anatomy the blood supply of the optic apparatus, namely, the of the OphA optic nerve and the retina, and the orbital branches supply the optic adnexae, such