الفهرس 
What is Visual Affection With Cerebrovascular Diseases?Only 14 pages are availabe for public view
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Abstract
A- whatisvisual affection in cerebrovascular diseases:
maurosisfugaxisthemostcommonocularsymptomin patients who had ocular ischemic diseases (47.44%)
(Jiangetal.,2010).
Etiology andpathophysiology ofamaurosisfugaxisvery complex. Inclassificationwe differentiate four types: angiospasm,retinal andcorticalvisualcenterhypoperfusion, embolic-thrombosiscausesandmigraine as idiopathic (Vojnikovic etal., 2010).
AIONcomprisesarteritic AION(A-AION: due togiantcell arteritis)andnon-arteriticAION (NA-AION:duetoother causes).PIONconsists of arteriticPION(A-PION:due togiant cellarteritis), non-arteriticPION(NA-PION:duetoother causes),andsurgicalPION(acomplicationof severalsystemic surgical procedures(Hayreh, 2011).
Corticalblindnesscaused bybilaterallesionsof the primary visualcortexinthe occipitallobes(Georgiosetal., 2010).
Terson’ssyndromeisintraocularhemorrhagesubsequent tosubarachnoidhemorrhage(Hassan etal., 2011).
Cerebrovascular disease in themidbrain simultaneously damagestheOculomotornervenucleusandotherneurofibers. It givesrise toa widerange of neurological symptomsas diplopia,manyofwhicharealreadywell-known(Osawaetal.,
2011).
Papilledemarefers to the swellingofthe optic nerve head secondarytoraisedcerebrospinalfluidpressure(Kedaretal.,
2011).
Ophthalmoplegicmigraine is achildhooddisorder of uncertainetiology manifestingrecurrentunilateralheadache associatedwithatransitoryoculomotorpalsy(Vieira etal.,
2008).
Thevascularetiology ofabilateralinternuclear ophthalmoplegia isan occlusion ofa unilateral paramedian pontine artery that may supply the medial longitudinal fasciculus(Araietal., 2011).
Embolism isthemostcommoncauseofcentralretinal artery occlusionandbranchartery occlusionplaqueinthe carotidarteryisusuallythesourceofembolism(Hayrehetal.,
2009).
Vision loss and ischaemic stroke are feared complications in Giant cell arteritis irrespective of platelet
countandsizeandestablishedAcetylsalicylicacidtreatment
(Bergeretal., 2009).
Visualillusionsandhallucinationscanoccurinrelation tolesionsinanypartof thevisualsystem(Gilligetal.,2009).
B-Clinicaldescriptionofvisualaffectionincerebro- vasculardiseases:
Amaurosis fugaxis used to describe any cause of transientmonocularvisualloss(Lamireletal., 2009).
Thediagnosis ofION ismadewhenconsideringmany factors.The patient is usually over 50years ofagewiththe complaintof sudden unilaterallossofvisionorhemi-fieldupon awakening(Hayreh etal.,2008).
Visualfield defectsinnonarteriticanterior ischemicoptic neuropathy includealtitudinalfielddefect,centralscotoma, arcuatescotoma,and quadrantic defects(Kedaretal., 2011).
Cortical blindnesspresentswith visual loss and limited eyelidclosureresponsetobrightlight, butanormalpupillary response andnormalfunduscopic examination(Habboushe et al., 2011).
SuspectedvisuallossfollowingSAH shouldprompta searchforTerson’ssyndromebyfunduscopy(Hassanetal.,
2011).
Transientbinocular horizontalor verticaldiplopiaisa commonmanifestation of vertebrobasilar ischemia(Lamirelet al., 2009).
Papilledemaischaracterizedby disc swelling, hemorrhages,andexudates(Gilligetal.,2009).
Mostof thecasescentralretinalartery occlusionpresent withpainlesssuddenpersistentlossofvisionintherange of countingfingersto perception oflight(Ghoseetal., 2011).
C-Theroleoffunduscopicexaminationincerebrov- asculardiseases:
Ocularfundusimagingplaysakey roleinmonitoringthe healthstatusof the humaneye (Bernardesetal., 2011).
Thenfundusexamination,visualacuity andvisualfield, fluoresceinangiography,andopticalcoherence tomography are performedinordertodifferentiate papilledemasecondary to increasedintracranialpressurefrom opticdisc swelling secondarytooptic neuropathy(Rougieretal., 2010).
Patientswiththediagnosis ofintracranialhaemorrhageshould besubmittedtoafunduscopicexamination(Sungetal.,2011).
Inanteriorischemicopticneuropathy Diffuseor segmental discedemaisobservedonfunduscopyatsymptomonset,with
thedevelopment ofopticnerve atrophyafter 4-8weeks(Berget al., 2010).
FunduscopicexaminationinCentralretinal vein occlusion revealsdiffusely spreadretinalsuperficialhemorrhages,retinal andmacularedema, dilatedandtortuous veins,andoptic disc edema.Cotton-wool spots suggestassociatedretinalischemia (Lamireletal.,2009).
D-treatment of visual affection in cerebrovascular disease:
Treatmentofamaurosisfugaxdependsonthe severity ofthe blockage inthe carotid artery. The goalof treatment is to preventastroke (Adamsetal.,2008).
Therapy forIONrevolvesaroundtherecommendationof systemic corticosteroidtherapy and intravitreal steroid injections(Hayreh etal., 2011).
Intreatmentsfor homonymousvisualfielddefectswe distinguish betweenthree treatments:visualrestoration training (VRT),opticalaids,andcompensatorytraining(Laneetal.,
2008).
Theadaptive gazestrategiesadoptedbycortically blind individualsasa compensationfor their visuallossare strongest and mosteffective when seated and stationary. Walking
significantly altersthesegazestrategiesinaway thatseemsto favorwalking performance, but impairsperipheraltarget detection(Iorizzo etal., 2011).
Nd:YAG laser treatmentisa non-invasive method,which enables the drainage ofthesubhyaloid hemorrhageinto the vitreouscavity(Erdurman etal., 2011).
Treatingapatientwithvisualfailure ordiplopiais challenging(Kiddetal., 2008).
Papilledemais oftentreatedwithcorticosteroids,alone or incombinationwithdiuretic therapy(Kiddetal.,2008).
In patientswithretinal vein occlusiontreatmentwith low molecularweight heparin seemsto beassociatedwith improvementinthevisualacuity andlessadverse ocular outcomes(Langneretal.,2010).
Prompttreatmentgiantcellarteritiswithcorticosteroids ledto preservation of visionandresolution of the retinal detachment(Ouaggagetal.,2011