Glaucoma - Wikipedia

Glaucoma · Glaucoma is a group of eye diseases that result in damage to the · Risk factors for glaucoma include increasing age, high · If treated early, it is ... Glaucoma FromWikipedia,thefreeencyclopedia Jumptonavigation Jumptosearch Eyediseaseinwhichhighintraocularpressuredamagestheopticnerve MedicalconditionGlaucomaAcuteangleclosureglaucomaofaperson'srighteye(shownatleft).Notethemid-sizedpupil,whichisnon-reactivetolight,andrednessofthewhitepartoftheeye.SpecialtyOphthalmology,optometrySymptomsVisionlosseyepainmid-dilatedpupilrednessoftheeyenausea[1][2]UsualonsetGradual,orsudden[2]RiskfactorsIncreasedpressureintheeye,familyhistory,highbloodpressure[1]DiagnosticmethodDilatedeyeexamination[1]DifferentialdiagnosisUveitis,trauma,keratitis,conjunctivitis[3]TreatmentMedication,laser,surgery[1]Frequency6–67million[2][4] Glaucomaisagroupofeyediseasesthatresultindamagetotheopticnerve(orretina[5])andcausevisionloss.[1]Themostcommontypeisopen-angle(wideangle,chronicsimple)glaucoma,inwhichthedrainageangleforfluidwithintheeyeremainsopen,withlesscommontypesincludingclosed-angle(narrowangle,acutecongestive)glaucomaandnormal-tensionglaucoma.[1]Open-angleglaucomadevelopsslowlyovertimeandthereisnopain.[1]Peripheralvisionmaybegintodecrease,followedbycentralvision,resultinginblindnessifnottreated.[1]Closed-angleglaucomacanpresentgraduallyorsuddenly.[2]Thesuddenpresentationmayinvolvesevereeyepain,blurredvision,mid-dilatedpupil,rednessoftheeye,andnausea.[1][2]Visionlossfromglaucoma,onceithasoccurred,ispermanent.[1]Eyesaffectedbyglaucomaarereferredtoasbeingglaucomatous. Riskfactorsforglaucomaincludeincreasingage,highpressureintheeye,afamilyhistoryofglaucoma,anduseofsteroidmedication.[1]Foreyepressures,avalueof21 mmHgor2.8 kPaaboveatmosphericpressure(760mmHg)isoftenused,withhigherpressuresleadingtoagreaterrisk.[2][6]However,somemayhavehigheyepressureforyearsandneverdevelopdamage.[2]Conversely,opticnervedamagemayoccurwithnormalpressure,knownasnormal-tensionglaucoma.[7]Themechanismofopen-angleglaucomaisbelievedtobetheslowexitofaqueoushumorthroughthetrabecularmeshwork,whileinclosed-angleglaucomatheirisblocksthetrabecularmeshwork.[2]Diagnosisisachievedbyperformingadilatedeyeexamination.[1]Often,theopticnerveshowsanabnormalamountofcupping.[2] Iftreatedearly,itispossibletosloworstoptheprogressionofdiseasewithmedication,lasertreatment,orsurgery.[1][8]Thegoalofthesetreatmentsistodecreaseeyepressure.[2]Anumberofdifferentclassesofglaucomamedicationareavailable.[2]Lasertreatmentsmaybeeffectiveinbothopen-angleandclosed-angleglaucoma.[2]Anumberoftypesofglaucomasurgeriesmaybeusedinpeoplewhodonotrespondsufficientlytoothermeasures.[2]Treatmentofclosed-angleglaucomaisamedicalemergency.[1] About70millionpeoplehaveglaucomaglobally,[2][4]withabouttwomillionpatientsintheUnitedStates.[2]ItistheleadingcauseofblindnessinAfricanAmericans.[9]Itoccursmorecommonlyamongolderpeople,[1]andclosed-angleglaucomaismorecommoninwomen.[2]Glaucomahasbeencalledthe"silentthiefofsight",becausethelossofvisionusuallyoccursslowlyoveralongperiodoftime.[10]Worldwide,glaucomaisthesecond-leadingcauseofblindnessaftercataracts.[2][11]Cataractscaused51%ofblindnessin2010,whileglaucomacaused8%.[12]Theword"glaucoma"isfromtheAncientGreekglaukos,whichmeans"shimmering."[13]InEnglish,thewordwasusedasearlyas1587butdidnotbecomecommonlyuseduntilafter1850,whenthedevelopmentoftheophthalmoscopealloweddoctorstoseetheopticnervedamage.[14] Contents 1Signsandsymptoms 2Causes 2.1Dietary 2.2Ethnicity 2.3Genetics 2.4Other 3Pathophysiology 4Diagnosis 4.1Primaryglaucomaanditsvariants 4.2Developmentalglaucoma 4.3Secondaryglaucoma 4.4Absoluteglaucoma 4.5Types 5Visualfielddefectsinglaucoma 6Screening 7Treatment 7.1Medication 7.2Laser 7.3Surgery 7.3.1Canaloplasty 7.3.2Trabeculectomy 7.3.3Glaucomadrainageimplants 7.3.4Laser-assistednonpenetratingdeepsclerectomy 7.3.5Lensextraction 8Prognosis 9Epidemiology 10History 10.1Etymology 11Research 11.1Rhokinaseinhibitors 11.2Neuroprotectiveagents 11.3Cannabis 12Healthdisparitiesinglaucoma 12.1Indiagnosis 12.2Intreatment 12.3Inresearchandclinicaltrials 13References 14Externallinks Signsandsymptoms[edit] Photoshowingconjunctivalvesselsdilatedatthecornealedge(ciliaryflush,circumcornealflush)andhazycorneacharacteristicofacuteangleclosureglaucoma Asopen-angleglaucomaisusuallypainlesswithnosymptomsearlyinthediseaseprocess,screeningthroughregulareyeexamsisimportant.Theonlysignsaregraduallyprogressivevisualfieldlossandopticnervechanges(increasedcup-to-discratioonfundoscopicexamination). About10%ofpeoplewithclosedanglespresentwithacuteangleclosurecharacterizedbysuddenocularpain,seeinghalosaroundlights,redeye,veryhighintraocularpressure(>30 mmHg(4.0 kPa)),nauseaandvomiting,suddenlydecreasedvision,andafixed,mid-dilatedpupil.Itisalsoassociatedwithanovalpupilinsomecases.Acuteangleclosureisanemergency. Opaquespecksmayoccurinthelensinglaucoma,knownasglaukomflecken.[15] Causes[edit] AnormalrangeofvisionThesameviewwithadvancedvisionlossfromglaucoma Ocularhypertension(increasedpressurewithintheeye)isthemostimportantriskfactorforglaucoma,butonlyabout50%ofpeoplewithprimaryopen-angleglaucomaactuallyhaveelevatedocularpressure.[16]Ocularhypertension—anintraocularpressureabovethetraditionalthresholdof21 mmHg(2.8 kPa)orevenabove24 mmHg(3.2 kPa)—isnotnecessarilyapathologicalcondition,butitincreasestheriskofdevelopingglaucoma.Onestudyfoundaconversionrateof18%withinfiveyears,meaningfewerthanoneinfivepeoplewithelevatedintraocularpressurewilldevelopglaucomatousvisualfieldlossoverthatperiodoftime.[17]Itisamatterofdebatewhethereverypersonwithanelevatedintraocularpressureshouldreceiveglaucomatherapy;currently,mostophthalmologistsfavortreatmentofthosewithadditionalriskfactors.[18] Open-angleglaucomaaccountsfor90%ofglaucomacasesintheUnitedStates.Closed-angleglaucomaaccountsforfewerthan10%ofglaucomacasesintheUnitedStates,butasmanyashalfofglaucomacasesinothernations(particularlyEastAsiancountries). Dietary[edit] Noclearevidenceindicatesthatvitamindeficienciescauseglaucomainhumans.Assuch,oralvitaminsupplementationisnotarecommendedtreatment.[19]Caffeineincreasesintraocularpressureinthosewithglaucoma,butdoesnotappeartoaffectnormalindividuals.[20] Ethnicity[edit] ManypeopleofEastAsiandescentarepronetodevelopingangleclosureglaucomabecauseofshalloweranteriorchamberdepths,withthemajorityofcasesofglaucomainthispopulationconsistingofsomeformofangleclosure.[21]HigherratesofglaucomahavealsobeenreportedforInuitpopulations,comparedtoWhitepopulations,inCanadaandGreenland.[citationneeded] Genetics[edit] Positivefamilyhistoryisariskfactorforglaucoma.Therelativeriskofhavingprimaryopen-angleglaucoma(POAG)isincreasedabouttwo-tofour-foldforpeoplewhohaveasiblingwithglaucoma.[22]Glaucoma,particularlyprimaryopen-angleglaucoma,isassociatedwithmutationsinseveralgenes,includingMYOC,ASB10,WDR36,NTF4,TBK1,[23]andRPGRIP1,[24]althoughmostcasesofglaucomadonotinvolvethesegeneticmutations.Normal-tensionglaucoma,whichcomprisesone-thirdofPOAG,isalsoassociatedwithgeneticmutations(includingOPA1andOPTNgenes).[25] Variousrarecongenital/geneticeyemalformationsareassociatedwithglaucoma.Occasionally,failureofthenormalthird-trimestergestationalatrophyofthehyaloidcanalandthetunicavasculosalentisisassociatedwithotheranomalies.Angleclosure-inducedocularhypertensionandglaucomatousopticneuropathymayalsooccurwiththeseanomalies[26][27][28]andhasbeenmodelledinmice.[29] Other[edit] Otherfactorscancauseglaucoma,knownas"secondaryglaucoma",includingprolongeduseofsteroids(steroid-inducedglaucoma);conditionsthatseverelyrestrictbloodflowtotheeye,suchasseverediabeticretinopathyandcentralretinalveinocclusion(neovascularglaucoma);oculartrauma(angle-recessionglaucoma);andinflammationofthemiddlelayerofthepigmentedvasculareyestructure(uveitis),knownasuveiticglaucoma. LaserDopplerimagingrevealsarterialbloodflowreversalinneovascularglaucoma.ThecolorchangeoftheDopplerimageinthecentralretinalarteryduringthecardiaccycleindicatesarterialflowreversal.[30] Pathophysiology[edit] Humaneyecross-sectionalview Theunderlyingcauseofopen-angleglaucomaremainsunclear.Severaltheoriesexistonitsexactetiology.However,themajorriskfactorformostglaucomasandthefocusoftreatmentisincreasedintraocularpressure.Intraocularpressureisafunctionofproductionofliquidaqueoushumorbytheciliaryprocessesoftheeye,anditsdrainagethroughthetrabecularmeshwork.Aqueoushumorflowsfromtheciliaryprocessesintotheposteriorchamber,boundedposteriorlybythelensandthezonulesofZinn,andanteriorlybytheiris.Itthenflowsthroughthepupiloftheirisintotheanteriorchamber,boundedposteriorlybytheirisandanteriorlybythecornea. Fromhere,thetrabecularmeshworkdrainsaqueoushumorviathescleralvenoussinus(Schlemm'scanal)intoscleralplexusesandgeneralbloodcirculation.[31] Inopen/wide-angleglaucoma,flowisreducedthroughthetrabecularmeshwork,duetothedegenerationandobstructionofthetrabecularmeshwork,whoseoriginalfunctionistoabsorbtheaqueoushumor.Lossofaqueoushumorabsorptionleadstoincreasedresistanceandthusachronic,painlessbuildupofpressureintheeye.[32] Inclose/narrow-angle,theiridocornealangleiscompletelyclosedbecauseofforwarddisplacementofthefinalrollandrootoftheirisagainstthecornea,resultingintheinabilityoftheaqueousfluidtoflowfromtheposteriortotheanteriorchamberandthenoutofthetrabecularnetwork.Thisaccumulationofaqueoushumorcausesanacuteincreaseinpressureandpain. Degenerationofaxonsoftheretinalganglioncells(theopticnerve)isahallmarkofglaucoma.[33]Theinconsistentrelationshipofglaucomatousopticneuropathywithincreasedintraocularpressurehasprovokedhypothesesandstudiesonanatomicstructure,eyedevelopment,nervecompressiontrauma,opticnervebloodflow,excitatoryneurotransmitter,trophicfactor,retinalganglioncell/axondegeneration,glialsupportcell,immunesystem,agingmechanismsofneuronloss,andseveringofthenervefibersatthescleraledge.[34][35][36][37][38][39][40][41][42][43][44] Diagnosis[edit] Opticnerveinadvancedglaucomadisease Screeningforglaucomaisusuallyperformedaspartofastandardeyeexaminationperformedbyoptometristsandophthalmologists.Testingforglaucomaincludesmeasurementsoftheintraocularpressureusingtonometry,[45]anteriorchamberangleexaminationorgonioscopyaswellasexaminationoftheopticnervetodiscernvisibledamage,changesinthecup-to-discratio,rimappearanceandvascularchange.Aformalvisualfieldtestisperformed.Theretinalnervefiberlayercanbeassessedwithimagingtechniquessuchasopticalcoherencetomography,scanninglaserpolarimetryorscanninglaserophthalmoscopy(Heidelbergretinaltomogram).[46][47][48]Visualfieldlossisthemostspecificsignofthecondition,thoughitoccurslaterinthecourseofthedisease.[49] Asallmethodsoftonometryaresensitivetocornealthickness,methodssuchasGoldmanntonometrymaybeaugmentedwithpachymetrytomeasurethecentralcornealthickness(CCT).Athickercorneacanresultinapressurereadinghigherthanthetruepressurebutathinnercorneacanproduceapressurereadinglowerthanthetruepressure.[50][medicalcitationneeded] Becausepressure-measurementerrorcanbecausedbymorethanjustCCT(suchasbycornealhydrationorelasticproperties),itisimpossibletoadjustpressuremeasurementsbasedonlyonCCTmeasurements.Thefrequency-doublingillusioncanalsobeusedtodetectglaucomawiththeuseofafrequency-doublingtechnologyperimeter.[50] Examinationforglaucomaisassessedwithattentiongiventogender,race,historyofdruguse,refraction,inheritanceandfamilyhistory.[46] Glaucomatests[51][52] Whatthetestexamines Eyedropsused Physicalcontactwiththeeye Procedure Tonometry Innereyepressure Maybe Maybe Eyedropsmaybeusedtonumbtheeye.Theexaminerthenusesatonometertomeasuretheinnerpressureoftheeyethroughpressureappliedbyapuffofwarmairoratinytool. Ophthalmoscopy(dilatedeyeexamination) Shapeandcoloroftheopticnerve Yes No Eyedropsareusedtodilatethepupil.Usingasmallmagnificationdevicewithalightontheend,theexaminercanexaminethemagnifiedopticnerve. Perimetry(visualfieldtest) Completefieldofvision No No Thepatientlooksstraightaheadandisaskedtoindicatewhenlightpassesthepatient'speripheralfieldofvision.Thisallowstheexaminertomapthepatient'sfieldofvision. Gonioscopy Angleintheeyewheretheirismeetsthecornea Yes Yes Eyedropsareusedtonumbtheeye.Ahand-heldcontactlenswithamirrorisplacedgentlyontheeyetoallowtheexaminertoseetheanglebetweenthecorneaandtheiris. Pachymetry Thicknessofthecornea No Yes Theexaminerplacesapachymetergentlyonthefrontoftheeyetomeasureitsthickness. Nervefiberanalysis Thicknessofthenervefiberlayer Maybe Maybe Usingoneofseveraltechniques,[clarificationneeded]thenervefibersareexamined. Glaucomahasbeenclassifiedintospecifictypes:[53] Primaryglaucomaanditsvariants[edit] Primaryglaucoma(H40.1-H40.2) Primaryopen-angleglaucoma,alsoknownaschronicopen-angleglaucoma,chronicsimpleglaucoma,glaucomasimplex High-tensionglaucoma Low-tensionglaucoma Primaryangleclosureglaucoma,alsoknownasprimaryclosed-angleglaucoma,narrow-angleglaucoma,pupil-blockglaucoma,acutecongestiveglaucoma Acuteangleclosureglaucoma(akaAACG)[54] Chronicangleclosureglaucoma Intermittentangleclosureglaucoma Superimposedonchronicopen-angleclosureglaucoma("combinedmechanism"–uncommon) Variantsofprimaryglaucoma Pigmentaryglaucoma Exfoliationglaucoma,alsoknownaspseudoexfoliativeglaucomaorglaucomacapsulare Primaryjuvenileglaucoma Primaryangleclosureglaucomaiscausedbycontactbetweentheirisandtrabecularmeshwork,whichinturnobstructsoutflowoftheaqueoushumorfromtheeye.Thiscontactbetweenirisandtrabecularmeshwork(TM)maygraduallydamagethefunctionofthemeshworkuntilitfailstokeeppacewithaqueousproduction,andthepressurerises.Inoverhalfofallcases,prolongedcontactbetweenirisandTMcausestheformationofsynechiae(effectively"scars"). Thesecausepermanentobstructionofaqueousoutflow.Insomecases,pressuremayrapidlybuildupintheeye,causingpainandredness(symptomatic,orso-called"acute"angleclosure).Inthissituation,thevisionmaybecomeblurred,andhalosmaybeseenaroundbrightlights.Accompanyingsymptomsmayincludeaheadacheandvomiting. Diagnosisismadefromphysicalsignsandsymptoms:pupilsmid-dilatedandunresponsivetolight,corneaedematous(cloudy),reducedvision,redness,andpain.However,themajorityofcasesareasymptomatic.Priortotheveryseverelossofvision,thesecasescanonlybeidentifiedbyexamination,generallybyaneyecareprofessional. Onceanysymptomshavebeencontrolled,thefirstline(andoftendefinitive)treatmentislaseriridotomy.ThismaybeperformedusingeitherNd:YAGorargonlasers,orinsomecasesbyconventionalincisionalsurgery.Thegoaloftreatmentistoreverseandpreventcontactbetweentheirisandtrabecularmeshwork.Inearlytomoderatelyadvancedcases,iridotomyissuccessfulinopeningtheangleinaround75%ofcases.Intheother25%,laseriridoplasty,medication(pilocarpine)orincisionalsurgerymayberequired. Primaryopen-angleglaucomaiswhenopticnervedamageresultsinaprogressivelossofthevisualfield.[55]Thisisassociatedwithincreasedpressureintheeye.Notallpeoplewithprimaryopen-angleglaucomahaveeyepressurethatiselevatedbeyondnormal,butdecreasingtheeyepressurefurtherhasbeenshowntostopprogressioneveninthesecases. Theincreasedpressureiscausedbytrabecularmeshworkblockage.Becausethemicroscopicpassagewaysareblocked,thepressurebuildsupintheeyeandcausesimperceptibleverygradualvisionloss.Peripheralvisionisaffectedfirst,buteventuallytheentirevisionwillbelostifnottreated. Diagnosisismadebylookingforcuppingoftheopticnerve.Prostaglandinagonistsworkbyopeninguveoscleralpassageways.Beta-blockers,suchastimolol,workbydecreasingaqueousformation.Carbonicanhydraseinhibitorsdecreasebicarbonateformationfromciliaryprocessesintheeye,thusdecreasingtheformationofaqueoushumor.Parasympatheticanalogsaredrugsthatworkonthetrabecularoutflowbyopeningupthepassagewayandconstrictingthepupil.Alpha2agonists(brimonidine,apraclonidine)bothdecreasefluidproduction(viainhibitionofAC)andincreasedrainage. Developmentalglaucoma[edit] Developmentalglaucoma(Q15.0) Primarycongenitalglaucoma Infantileglaucoma Glaucomaassociatedwithhereditaryorfamilialdiseases Secondaryglaucoma[edit] Secondaryglaucoma(H40.3-H40.6) Inflammatoryglaucoma Uveitisofalltypes Fuchsheterochromiciridocyclitis Phacogenicglaucoma Angle-closureglaucomawithmaturecataract Phacoanaphylacticglaucomasecondarytoruptureoflenscapsule Phacolyticglaucomaduetophacotoxicmeshworkblockage Subluxationoflens Glaucomasecondarytointraocularhemorrhage Hyphema Hemolyticglaucoma,alsoknownaserythroclasticglaucoma Traumaticglaucoma Anglerecessionglaucoma:Traumaticrecessiononanteriorchamberangle Postsurgicalglaucoma Aphakicpupillaryblock Ciliaryblockglaucoma Neovascularglaucoma(seebelowformoredetails) Drug-inducedglaucoma Corticosteroidinducedglaucoma Alpha-chymotrypsinglaucoma.Postoperativeocularhypertensionfromuseofalphachymotrypsin. Glaucomaofmiscellaneousorigin Associatedwithintraoculartumors Associatedwithretinaldetachments Secondarytoseverechemicalburnsoftheeye Associatedwithessentialirisatrophy Toxicglaucoma Neovascularglaucoma,anuncommontypeofglaucoma,isdifficultornearlyimpossibletotreat,andisoftencausedbyproliferativediabeticretinopathy(PDR)orcentralretinalveinocclusion(CRVO).Itmayalsobetriggeredbyotherconditionsthatresultinischemiaoftheretinaorciliarybody.Individualswithpoorbloodflowtotheeyearehighlyatriskforthiscondition. Neovascularglaucomaresultswhennew,abnormalvesselsbegindevelopingintheangleoftheeyethatbeginblockingthedrainage.Peoplewithsuchconditionbegintorapidlylosetheireyesight.Sometimes,thediseaseappearsveryrapidly,especiallyaftercataractsurgeryprocedures.Anewtreatmentforthisdisease,asfirstreportedbyKahookandcolleagues,involvestheuseofanovelgroupofmedicationsknownasanti-VEGFagents.Theseinjectablemedicationscanleadtoadramaticdecreaseinnewvesselformationand,ifinjectedearlyenoughinthediseaseprocess,mayleadtonormalizationofintraocularpressure.Currently,therearenohigh-qualitycontrolledtrialsdemonstratingabeneficialeffectofanti-VEGFtreatmentsinloweringIOPinpeoplewithneovascularglaucoma.[56] Toxicglaucomaisopen-angleglaucomawithanunexplainedsignificantriseofintraocularpressurefollowingunknownpathogenesis.Intraocularpressurecansometimesreach80 mmHg(11 kPa).ItcharacteristicallymanifestsasciliarybodyinflammationandmassivetrabecularoedemathatsometimesextendstoSchlemm'scanal.Thisconditionisdifferentiatedfrommalignantglaucomabythepresenceofadeepandclearanteriorchamberandalackofaqueousmisdirection.Also,thecornealappearanceisnotashazy.Areductioninvisualacuitycanoccurfollowedneuroretinalbreakdown. Associatedfactorsincludeinflammation,drugs,traumaandintraocularsurgery,includingcataractsurgeryandvitrectomyprocedures.GedePardianto(2005)reportedonfourpatientswhohadtoxicglaucoma.Oneofthemunderwentphacoemulsificationwithsmallparticlenucleusdrops.Somecasescanberesolvedwithsomemedication,vitrectomyproceduresortrabeculectomy.Valvingprocedurescangivesomerelief,butfurtherresearchisrequired.[57] Absoluteglaucoma[edit] Absoluteglaucoma(H44.5)istheendstageofalltypesofglaucoma.Theeyehasnovision,absenceofpupillarylightreflexandpupillaryresponse,andhasastonyappearance.Severepainispresentintheeye.Thetreatmentofabsoluteglaucomaisadestructiveprocedurelikecyclocryoapplication,cyclophotocoagulation,orinjectionof99%alcohol. Types[edit] Thissectionneedsadditionalcitationsforverification.Pleasehelpimprovethisarticlebyaddingcitationstoreliablesources.Unsourcedmaterialmaybechallengedandremoved.(August2015)(Learnhowandwhentoremovethistemplatemessage) Glaucomaisanumbrellatermforeyeconditionsthatdamagetheopticnerveandthatcanleadtoalossofvision.[58]Themaincauseofdamagetotheopticnerveisintraocularpressure(IOP),excessivefluidpressurewithintheeye,whichcanbecausedbyfactorssuchasblockageofdrainageductsandnarrowingorclosureoftheanglebetweentheirisandcornea. Glaucomaisprimarilycategorizedaseitheropen-angleorclosed-angle(orangle-closure).Inopen-angleglaucoma,theirismeetsthecorneanormally,allowingthefluidfrominsidetheeyetodrain,thusrelievingtheinternalpressure.Whenthisangleisnarrowedorclosed,pressureincreasesovertime,causingdamagetotheopticnerveandleadingtoblindness. Primaryopen-angleglaucoma(alsocalledprimaryorchronicglaucoma)involvestheslowcloggingofdrainagecanalsresultinginincreasedeyepressure,whichcausesprogressiveopticnervedamage.Thismanifestsasagraduallossofthevisualfield,startingwithalossofperipheralvision,buteventuallyallvisionwillbelostiftheconditionisnottreated.[55]Thisisthemostcommontypeofglaucoma,accountingfor90%ofcasesintheUnitedStates,butislessprevalentinAsiancountries.Onsetisslowandpainless,andlossofvisionisgradualandirreversible. Withnarrow-angleglaucoma(alsocalledclosed-angleglaucoma),theirisbowsforward,narrowingtheanglethatdrainstheeye,increasingpressurewithintheeye.Ifuntreated,itcanleadtothemedicalemergencyofangle-closureglaucoma. Withangle-closureglaucoma(alsocalledclosed-angle,primaryangle-closureoracuteglaucoma),theirisbowsforwardandcausesphysicalcontactbetweentheirisandtrabecularmeshwork,whichblockstheoutflowofaqueoushumorfromwithintheeye.Thiscontactmaygraduallydamagethedrainingfunctionofthemeshworkuntilitfailstokeeppacewithaqueousproduction,andtheintraocularpressurerises.Theonsetofsymptomsissuddenandcausespainandothernoticeablesymptoms,andtheconditionistreatedasamedicalemergency.Unlikeopen-angleglaucoma,angle-closureglaucomaisaresultoftheclosingoftheanglebetweentheirisandcornea.Thistendstooccurinthefarsighted,whohavesmalleranteriorchambers,makingphysicalcontactbetweentheirisandtrabecularmeshworkmorelikely.Avarietyoftestsmaybeperformedtodetectthoseatriskofangle-closureglaucoma.[59] Normal-tensionglaucoma(NTG,alsocalledlow-tensionornormal-pressureglaucoma)isaconditioninwhichtheopticnerveisdamagedalthoughintraocularpressure(IOP)isinthenormalrange(12to22 mmHg(1.6to2.9 kPa)).IndividualswithafamilyhistoryofNTG,thoseofJapaneseancestry,thosewithahistoryofsystemicheartdiseaseandthosewithFlammersyndromeareatanelevatedriskofdevelopingNTG.ThecauseofNTGisunknown. Secondaryglaucomareferstoanycaseinwhichanotherdisease,trauma,drugorprocedurecausesincreasedeyepressure,resultinginopticnervedamageandvisionloss,whichmaybemildorsevere.Thismaybetheresultofaneyeinjury,inflammation,atumororadvancedcasesofcataractsordiabetes.Itcanalsobecausedbycertaindrugssuchassteroids.Treatmentdependsonwhethertheconditionisidentifiedasopen-angleorangle-closureglaucoma. Withpseudoexfoliationglaucoma(alsoknownasPEXorexfoliationglaucoma)thepressureresultsfromtheaccumulationofmicroscopicgranularproteinfibers,whichcanblocknormaldrainageoftheaqueoushumor.PEXisprevalentinScandinavia,primarilyinthoseover70,andmorecommonlyinwomen. Pigmentaryglaucoma(alsoknownaspigmentarydispersionsyndrome)iscausedbypigmentcellssloughingofffromthebackoftheirisandfloatingaroundintheaqueoushumor.Overtime,thesepigmentcellscanaccumulateintheanteriorchamberandbegintoclogthetrabecularmeshwork.Itisarareconditionthatoccursmostlyamongwhitemalesintheirmid-20sto40s,mostofwhomarenearsighted. Primaryjuvenileglaucomaisaneonateorjuvenileabnormalityinwhichocularhypertensionisevidentatbirthorshortlythereafterandiscausedbyabnormalitiesintheanteriorchamberangledevelopmentthatblockstheoutflowoftheaqueoushumor. Uveiticglaucomaiscausedbyuveitis,theswellingandinflammationoftheuvea,themiddlelayeroftheeye.Theuveaprovidesmostofthebloodsupplytotheretina.Increasedeyepressurecanresultfromtheinflammationitselforfromthesteroidsusedtotreatit.[60] Visualfielddefectsinglaucoma[edit] Seealso:Visualfield Bjerrumsareaandtypesofscotomasonthevisualfield Inglaucomavisualfielddefectsresultfromdamagetotheretinalnervefiberlayer.Fielddefectsareseenmainlyinprimaryopenangleglaucoma.BecauseoftheuniqueanatomyoftheRNFL,manynoticeablepatternsareseeninthevisualfield.Mostoftheearlyglaucomatouschangesareseenwithinthecentralvisualfield,mainlyinBjerrum'sarea,10-20°fromfixation.[61] Followingarethecommonglaucomatousfielddefects: Generalizeddepression:Generalizeddepressionisseeninearlystagesofglaucomaandmanyotherconditions.Mildconstrictionofcentralandperipheralvisualfieldduetoisoptercontractioncomesundergeneralizeddepression.Ifalltheisoptersshowsimilardepressiontothesamepoint,itisthencalledacontractionofvisualfield.Relativeparacentralscotomasaretheareaswheresmalleranddimmertargetsarenotvisualizedbythepatient.[61]Largerandbrightertargetscanbeseen.Smallparacentraldepressions,mainlysuperonasalareseeninnormaltensionglaucoma(NTG).[62]Thegeneralizeddepressionoftheentirefieldmaybeseenincataractalso.[63] Baringofblindspot:"Baringofblindspot"meansexclusionofblindspotfromthecentralfieldduetoinwardcurveoftheouterboundaryof30°centralfield.[64]Itisonlyanearlynon-specificvisualfieldchange,withoutmuchdiagnosticvalueinglaucoma.[64] Smallwing-shapedParacentralscotoma:Smallwing-shapedParacentralscotomawithinBjerrum'sareaistheearliestclinicallysignificantfielddefectseeninglaucoma.Itmayalsobeassociatedwithnasalsteps.Scotomamaybeseenaboveorbelowtheblindspot.[64] Siedel'ssickle-shapedscotoma:ParacentralscotomajoinswiththeblindspottoformtheSeidelsign. ArcuateorBjerrum'sscotoma:ArcuatescotomaItisformedatlaterstagesofglaucomabyextensionofSeidel'sscotomainanareaeitheraboveorbelowthefixationpointtoreachthehorizontalline.Peripheralbreakthroughmayoccurduetodamageofnervefibers.[64] RingorDoublearcuatescotoma:TwoarcuatescotomasjointoformaRingorDoublearcuatescotoma.Thisdefectisseeninadvancedstagesofglaucoma. Roenne'scentralnasalstep:Itiscreatedwhentwoarcuatescotomasrunindifferentarcstoformarightangleddefect.Thisisalsoseeninadvancedstagesofglaucoma. Peripheralfielddefects:Peripheralfielddefectsmayoccurinearlyorlatestagesofglaucoma.Roenne'speripheralnasalstepsoccurduetocontractionofperipheralisopter.[64] Tubularvision:TubularvisionSincemacularfibersarethemostresistanttoglaucomatousdamage,thecentralvisionremainsunaffecteduntilendstagesofglaucoma.TubularvisionorTunnelvisionisthelossofperipheralvisionwithretentionofcentralvision,resultinginaconstrictedcirculartunnel-likefieldofvision.Itisseenintheendstagesofglaucoma.Retinitispigmentosaisanotherdiseasethatcausestubularvision.[65] Temporalislandofvision:Itisalsoseeninendstagesofglaucoma.Thetemporalislandslieoutsideofthecentral24to30°visualfield,[66]soitmaynotbevisiblewithstandardcentralfieldmeasurementsdoneinglaucoma. Screening[edit] TheUnitedStatesPreventiveServicesTaskForcestated,asof2013,thattherewasinsufficientevidencetorecommendfororagainstscreeningforglaucoma.[67]Therefore,thereisnonationalscreeningprogramintheUS.Screening,however,isrecommendedstartingatage40bytheAmericanAcademyofOphthalmology.[2] ThereisaglaucomascreeningprogramintheUK.Thoseatriskareadvisedtohaveadilatedeyeexaminationatleastonceayear.[68] Treatment[edit] Themoderngoalsofglaucomamanagementaretoavoidglaucomatousdamageandnervedamage,andpreservevisualfieldandtotalqualityoflifeforpatients,withminimalside-effects.[69][70]Thisrequiresappropriatediagnostictechniquesandfollow-upexaminations,andjudiciousselectionoftreatmentsfortheindividualpatient.Althoughintraocularpressure(IOP)isonlyoneofthemajorriskfactorsforglaucoma,loweringitviavariouspharmaceuticalsand/orsurgicaltechniquesiscurrentlythemainstayofglaucomatreatment.Areviewofpeoplewithprimaryopen-angleglaucomaandocularhypertensionconcludedthatmedicalIOP-loweringtreatmentsloweddowntheprogressionofvisualfieldloss.[8] Vascularflowandneurodegenerativetheoriesofglaucomatousopticneuropathyhavepromptedstudiesonvariousneuroprotectivetherapeuticstrategies,includingnutritionalcompounds,someofwhichmayberegardedbycliniciansassafeforusenow,whileothersareontrial.[citationneeded]Mentalstressisalsoconsideredasconsequenceandcauseofvisionlosswhichmeansthatstressmanagementtraining,autogenictrainingandothertechniquestocopewithstresscanbehelpful.[71] Medication[edit] Mainarticle:Glaucomamedication Intraocularpressurecanbeloweredwithmedication,usuallyeyedrops.Severalclassesofmedicationsareusedtotreatglaucoma,withseveralmedicationsineachclass. Eachofthesemedicinesmayhavelocalandsystemicsideeffects.Adherencetomedicationprotocolcanbeconfusingandexpensive;ifsideeffectsoccur,thepatientmustbewillingeithertotoleratethemortocommunicatewiththetreatingphysiciantoimprovethedrugregimen.Initially,glaucomadropsmayreasonablybestartedineitheroneorinbotheyes.[72]Wipingtheeyewithanabsorbentpadaftertheadministrationofeyedropsmayresultinfeweradverseeffects,likethegrowthofeyelashesandhyperpigmentationintheeyelid.[73] Poorcompliancewithmedicationsandfollow-upvisitsisamajorreasonforvisionlossinglaucomapatients.A2003studyofpatientsinanHMOfoundhalffailedtofilltheirprescriptionsthefirsttime,andone-quarterfailedtorefilltheirprescriptionsasecondtime.[74]Patienteducationandcommunicationmustbeongoingtosustainsuccessfultreatmentplansforthislifelongdiseasewithnoearlysymptoms. Thepossibleneuroprotectiveeffectsofvarioustopicalandsystemicmedicationsarealsobeinginvestigated.[19][75][76][77] Prostaglandinanalogs,suchaslatanoprost,bimatoprostandtravoprost,increaseuveoscleraloutflowofaqueoushumor.Bimatoprostalsoincreasestrabecularoutflow. Topicalbeta-adrenergicreceptorantagonists,suchastimolol,levobunolol,andbetaxolol,decreaseaqueoushumorproductionbytheepitheliumoftheciliarybody. Alpha2-adrenergicagonists,suchasbrimonidineandapraclonidine,workbyadualmechanism,decreasingaqueoushumorproductionandincreasinguveoscleraloutflow. Less-selectivealphaagonists,suchasepinephrine,decreaseaqueoushumorproductionthroughvasoconstrictionofciliarybodybloodvessels,usefulonlyinopen-angleglaucoma.Epinephrine'smydriaticeffect,however,rendersitunsuitableforclosed-angleglaucomaduetofurthernarrowingoftheuveoscleraloutflow(i.e.furtherclosureoftrabecularmeshwork,whichisresponsibleforabsorptionofaqueoushumor). Mioticagents(parasympathomimetics),suchaspilocarpine,workbycontractionoftheciliarymuscle,openingthetrabecularmeshworkandallowingincreasedoutflowoftheaqueoushumour.Echothiophate,anacetylcholinesteraseinhibitor,isusedinchronicglaucoma. Carbonicanhydraseinhibitors,suchasdorzolamide,brinzolamide,andacetazolamide,lowersecretionofaqueoushumorbyinhibitingcarbonicanhydraseintheciliarybody. Laser[edit] Argonlasertrabeculoplasty(ALT)maybeusedtotreatopen-angleglaucoma,butthisisatemporarysolution,notacure.A50-μmargonlaserspotisaimedatthetrabecularmeshworktostimulatetheopeningofthemeshtoallowmoreoutflowofaqueousfluid.Usually,halfoftheangleistreatedatatime.Traditionallasertrabeculoplastyusesathermalargonlaserinanargonlasertrabeculoplastyprocedure. Nd:YAGlaserperipheraliridotomy(LPI)maybeusedinpatientssusceptibletooraffectedbyangleclosureglaucomaorpigmentdispersionsyndrome.Duringlaseriridotomy,laserenergyisusedtomakeasmall,full-thicknessopeningintheiristoequalizethepressurebetweenthefrontandbackoftheiris,thuscorrectinganyabnormalbulgingoftheiris.Inpeoplewithnarrowangles,thiscanuncoverthetrabecularmeshwork.Insomecasesofintermittentorshort-termangleclosure,thismaylowertheeyepressure.Laseriridotomyreducestheriskofdevelopinganattackofacuteangleclosure.Inmostcases,italsoreducestheriskofdevelopingchronicangleclosureorofadhesionsoftheiristothetrabecularmeshwork. DiodelasercycloablationlowersIOPbyreducingaqueoussecretionbydestroyingsecretoryciliaryepithelium.[46] Surgery[edit] Conventionalsurgerytotreatglaucomamakesanewopeninginthetrabecularmeshwork,whichhelpsfluidtoleavetheeyeandlowersintraocularpressure. Mainarticle:Glaucomasurgery Bothlaserandconventionalsurgeriesareperformedtotreatglaucoma.Surgeryistheprimarytherapyforthosewithcongenitalglaucoma.[78]Generally,theseoperationsareatemporarysolution,asthereisnotyetacureforglaucoma. Canaloplasty[edit] Canaloplastyisanonpenetratingprocedureusingmicrocathetertechnology.Toperformacanaloplasty,anincisionismadeintotheeyetogainaccesstotheSchlemm'scanalinasimilarfashiontoaviscocanalostomy.Amicrocatheterwillcircumnavigatethecanalaroundtheiris,enlargingthemaindrainagechannelanditssmallercollectorchannelsthroughtheinjectionofasterile,gel-likematerialcalledviscoelastic.Thecatheteristhenremovedandasutureisplacedwithinthecanalandtightened. Byopeningthecanal,thepressureinsidetheeyemayberelieved,althoughthereasonisunclear,sincethecanal(ofSchlemm)doesnothaveanysignificantfluidresistanceinglaucomaorhealthyeyes.Long-termresultsarenotavailable.[79][80] Trabeculectomy[edit] Themostcommonconventionalsurgeryperformedforglaucomaisthetrabeculectomy.Here,apartialthicknessflapismadeinthescleralwalloftheeye,andawindowopeningismadeundertheflaptoremoveaportionofthetrabecularmeshwork.Thescleralflapisthensuturedlooselybackinplacetoallowfluidtoflowoutoftheeyethroughthisopening,resultinginloweredintraocularpressureandtheformationofableborfluidbubbleonthesurfaceoftheeye. Scarringcanoccuraroundorovertheflapopening,causingittobecomelesseffectiveorloseeffectivenessaltogether.Traditionally,chemotherapeuticadjuvants,suchasmitomycinC(MMC)or5-fluorouracil(5-FU),areappliedwithsoakedspongesonthewoundbedtopreventfilteringblebsfromscarringbyinhibitingfibroblastproliferation.ContemporaryalternativestopreventthescarringofthemeshworkopeningincludethesoleorcombinativeimplementationofnonchemotherapeuticadjuvantssuchastheOlogencollagenmatrix,whichhasbeenclinicallyshowntoincreasethesuccessratesofsurgicaltreatment.[81][82][83][84] Collagenmatrixpreventsscarringbyrandomizingandmodulatingfibroblastproliferationinadditiontomechanicallypreventingwoundcontractionandadhesion. Glaucomadrainageimplants[edit] Mainarticle:Glaucomavalve Thefirstglaucomadrainageimplantwasdevelopedin1966.[85]Sincethen,severaltypesofimplantshavefollowedonfromtheoriginal:theBaerveldttubeshunt,orthevalvedimplants,suchastheAhmedglaucomavalveimplantortheExPressMiniShuntandthelatergenerationpressureridgeMoltenoimplants.Theseareindicatedforglaucomapatientsnotrespondingtomaximalmedicaltherapy,withpreviousfailedguardedfilteringsurgery(trabeculectomy).Theflowtubeisinsertedintotheanteriorchamberoftheeye,andtheplateisimplantedunderneaththeconjunctivatoallowaflowofaqueousfluidoutoftheeyeintoachambercalledableb. Thefirst-generationMoltenoandothernonvalvedimplantssometimesrequiretheligationofthetubeuntiltheblebformedismildlyfibrosedandwater-tight.[86]Thisisdonetoreducepostoperativehypotony—suddendropsinpostoperativeintraocularpressure. Valvedimplants,suchastheAhmedglaucomavalve,attempttocontrolpostoperativehypotonybyusingamechanicalvalve. Abinternoimplants,suchastheXenGelStent,aretransscleralimplantsbyanabinternoproceduretochannelaqueoushumorintothenon-dissectedTenon'sspace,creatingasubconjunctivaldrainageareasimilartoableb.[87][88]Theimplantsaretransscleralanddifferentfromotherabinternoimplantsthatdonotcreateatransscleraldrainage,suchasiStent,CyPass,orHydrus.[89][90] Theongoingscarringovertheconjunctivaldissipationsegmentoftheshuntmaybecometoothickfortheaqueoushumortofilterthrough.Thismayrequirepreventivemeasuresusingantifibroticmedications,suchas5-fluorouracilormitomycin-C(duringtheprocedure),orothernonantifibroticmedicationmethods,suchascollagenmatriximplant,[91][92]orbiodegradablespacer,orlateroncreateanecessityforrevisionsurgerywiththesoleorcombinativeuseofdonorpatchgraftsorcollagenmatriximplant.[92]Andforglaucomatouspainfulblindeyeandsomecasesofglaucoma,cyclocryotherapyforciliarybodyablationcouldbeconsideredtobeperformed.[46] Laser-assistednonpenetratingdeepsclerectomy[edit] Themostcommonsurgicalapproachcurrentlyusedforthetreatmentofglaucomaistrabeculectomy,inwhichthescleraispuncturedtoalleviateintraocularpressure. Nonpenetratingdeepsclerectomy(NPDS)surgeryisasimilar,butmodified,procedure,inwhichinsteadofpuncturingthescleralbedandtrabecularmeshworkunderascleralflap,aseconddeepscleralflapiscreated,excised,withfurtherproceduresofderoofingtheSchlemm'scanal,uponwhich,percolationofliquidfromtheinnereyeisachievedandthusalleviatingintraocularpressure,withoutpenetratingtheeye.NPDSisdemonstratedtohavesignificantlyfewersideeffectsthantrabeculectomy.[93]However,NPDSisperformedmanuallyandrequireshigherlevelofskillsthatmaybeassistedwithinstruments.[citationneeded]Inordertopreventwoundadhesionafterdeepscleralexcisionandtomaintaingoodfilteringresults,NPDSaswithothernon-penetratingproceduresissometimesperformedwithavarietyofbiocompatiblespacersordevices,suchastheAquaflowcollagenwick,[94]ologenCollagenMatrix,[83][95][96]orXenoplastglaucomaimplant.[97] Laser-assistedNPDSisperformedwiththeuseofaCO2lasersystem.Thelaser-basedsystemisself-terminatingoncetherequiredscleralthicknessandadequatedrainageoftheintraocularfluidhavebeenachieved.Thisself-regulationeffectisachievedastheCO2laseressentiallystopsablatingassoonasitcomesincontactwiththeintraocularpercolatedliquid,whichoccursassoonasthelaserreachestheoptimalresidualintactlayerthickness. Lensextraction[edit] Forpeoplewithchronicclosed-angleglaucoma,lensextractioncanrelievetheblockcreatedbythepupilandhelpregulatetheintraocularpressure.[98] Prognosis[edit] Inopen-angleglaucoma,thetypicalprogressionfromnormalvisiontocompleteblindnesstakesabout25yearsto70yearswithouttreatment,dependingonthemethodofestimationused.[99]Theintraocularpressurecanalsohaveaneffect,withhigherpressuresreducingthetimeuntilblindness.[100] Epidemiology[edit] Disability-adjustedlifeyearforglaucomaper100,000 inhabitantsin2004[101]  nodata  fewerthan20  20–43  43–66  66–89  89–112  112–135  135–158  158–181  181–204  204–227  227–250  morethan250 Asof2010,therewere44.7millionpeopleintheworldwithopenangleglaucoma.[102]Thesameyear,therewere2.8millionpeopleintheUnitedStateswithopenangleglaucoma.[102]By2020,theprevalenceisprojectedtoincreaseto58.6millionworldwideand3.4millionintheUnitedStates.[102] BothinternationallyandintheUnitedStates,glaucomaisthesecond-leadingcauseofblindness.[2]Globally,cataractsareamorecommoncause.GlaucomaisalsotheleadingcauseofblindnessinAfricanAmericans,whohavehigherratesofprimaryopen-angleglaucoma.[103][104]Bilateralvisionlosscannegativelyaffectmobilityandinterferewithdriving.[105] Ameta-analysispublishedin2009foundthatpeoplewithprimaryopenangleglaucomadonothaveincreasedmortalityrates,orincreasedriskofcardiovasculardeath.[106] History[edit] Theassociationofelevatedintraocularpressure(IOP)andglaucomawasfirstdescribedbyEnglishmanRichardBannisterin1622:"...thattheEyebegrownmoresolidandhard,thennaturallyitshouldbe...".[107]Angle-closureglaucomawastreatedwithcataractextractionbyJohnCollinsWarreninBostonasearlyas1806.[108]TheinventionoftheophthalmoscopebyHermannHelmholtzin1851enabledophthalmologistsforthefirsttimetoidentifythepathologicalhallmarkofglaucoma,theexcavationoftheopticnerveheadduetoretinalganglioncellloss.ThefirstreliableinstrumenttomeasureintraocularpressurewasinventedbyNorwegianophthalmologistHjalmarAugustSchiøtzin1905.Abouthalfacenturylater,HansGoldmanninBerne,Switzerland,developedhisapplanationtonometerwhichstilltoday-despitenumerousnewinnovationsindiagnostics-isconsideredthegoldstandardofdeterminingthiscrucialpathogenicfactor.Inthelate20thcentury,furtherpathomechanismsbeyondelevatedIOPwerediscoveredandbecamethesubjectofresearchlikeinsufficientbloodsupply–oftenassociatedwithloworirregularbloodpressure–totheretinaandopticnervehead.[109]ThefirstdrugtoreduceIOP,pilocarpine,wasintroducedinthe1870s;othermajorinnovationsinpharmacologicalglaucomatherapyweretheintroductionofbetablockereyedropsinthe1970sandofprostaglandinanaloguesandtopical(locallyadministered)carbonicanhydraseinhibitorsinthemid-1990s..Earlysurgicaltechniqueslikeiridectomyandfistulatingmethodshaverecentlybeensupplementedbylessinvasiveprocedureslikesmallimplants,arangeofoptionsnowwidelycalledMIGS(micro-invasiveglaucomasurgery). Etymology[edit] Theword"glaucoma"comesfromtheAncientGreekγλαύκωμα,[110]aderivativeofγλαυκóς,[111]whichcommonlydescribedthecolorofeyeswhichwerenotdark(i.e.blue,green,lightgray).EyesdescribedasγλαυκóςduetodiseasemighthavehadagraycataractintheHippocraticera,or,intheearlyCommonEra,thegreenishpupillaryhuesometimesseeninangle-closureglaucoma.[112][113] Research[edit] Scientiststrackeyemovementsinglaucomapatientstocheckvisionimpairmentwhiledriving Rhokinaseinhibitors[edit] Rhokinaseinhibitors,suchasripasudil,workbyinhibitionoftheactincytoskeleton,resultinginthemorphologicalchangesinthetrabecularmeshworkandincreasedaqueousoutflow.Morecompoundsinthisclassarebeinginvestigatedinphase2andphase3trials.[114] Neuroprotectiveagents[edit] A2013CochraneSystematicReviewcomparedtheeffectofbrimonidineandtimololinslowingtheprogressionofopenangleglaucomainadultparticipants.[115]Theresultsshowedthatparticipantsassignedtobrimonidineshowedlessvisualfieldprogressionthanthoseassignedtotimolol,thoughtheresultswerenotsignificant,giventheheavyloss-to-followupandlimitedevidence.[115]Themeanintraocularpressuresforbothgroupsweresimilar.Participantsinthebrimonidinegrouphadahigheroccurrenceofsideeffectscausedbymedicationthanparticipantsinthetimololgroup.[115] Cannabis[edit] Studiesinthe1970sreportedthattheuseofcannabismaylowerintraocularpressure.[116][117]Inanefforttodeterminewhethermarijuana,ordrugsderivedfromit,mightbeeffectiveasaglaucomatreatment,theUSNationalEyeInstitutesupportedresearchstudiesfrom1978to1984.Thesestudiesdemonstratedsomederivativesofmarijuanaloweredintraocularpressurewhenadministeredorally,intravenously,orbysmoking,butnotwhentopicallyappliedtotheeye. In2003,theAmericanAcademyofOphthalmologyreleasedapositionstatementstatingthatcannabiswasnotmoreeffectivethanprescriptionmedications.Furthermore,noscientificevidencehasbeenfoundthatdemonstratesincreasedbenefitsand/ordiminishedrisksofcannabisusetotreatglaucomacomparedwiththewidevarietyofpharmaceuticalagentsnowavailable.[117][118] In2010theAmericanGlaucomaSocietypublishedapositionpaperdiscreditingtheuseofcannabisasalegitimatetreatmentforelevatedintraocularpressure,forreasonsincludingshortdurationofactionandsideeffectsthatlimitmanyactivitiesofdailyliving.[119] Healthdisparitiesinglaucoma[edit] Indiagnosis[edit] AstudyconductedinUKshowedthatpeoplelivinginanareaofhighdeprivationwerelikelytobediagnosedinthelaterstageofthedisease.[120]Italsoshowedthattherewerelackofprofessionalophthalmicservicesintheareaofhighdeprivation. Intreatment[edit] Astudyin2017showsthatthereisahugedifferenceinthevolumeofglaucomatestingdependingonthetypeofinsuranceintheUS.[121]Researchersreviewed21,766personsage≥40yearsoldwithnewlydiagnosedopen-angleglaucoma(OAG)andfoundthatMedicaidrecipientshadsubstantiallylowervolumeofglaucomatestingperformedcomparedtopatientswithcommercialhealthinsurance. Inresearchandclinicaltrials[edit] Resultsfromameta-analysisof33,428primaryopen-angleglaucoma(POAG)participantspublishedin2021suggestthattherearesubstantialethnicandracialdisparitiesinclinicaltrialsintheUS.[122]Althoughethnicandracialminoritieshaveahigherdiseaseburden,the70.7%ofthestudyparticipantswasWhiteasopposedto16.8%Blackand3.4%Hispanic/Latino. 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Externallinks[edit] Medicineportal GlaucomaatCurlie GeneReview/NCBI/NIH/UWentryonPrimaryCongenitalGlaucoma ClassificationDICD-10:H40-H42ICD-9-CM:365MeSH:D005901DiseasesDB:5226ExternalresourcesMedlinePlus:001620eMedicine:oph/578 vteDiseasesofthehumaneyeAdnexaEyelidInflammation Stye Chalazion Blepharitis Meibomianglanddysfunction Entropion Ectropion Lagophthalmos Blepharochalasis Ptosis Blepharophimosis Xanthelasma Ankyloblepharon Eyelash Trichiasis Madarosis Lacrimalapparatus Dacryoadenitis Epiphora Dacryocystitis Xerophthalmia Orbit Exophthalmos Enophthalmos Orbitalcellulitis Orbitallymphoma Periorbitalcellulitis Conjunctiva Conjunctivitis allergic Pterygium Pseudopterygium Pinguecula Subconjunctivalhemorrhage GlobeFibroustunicSclera Scleritis Episcleritis Cornea Keratitis herpetic acanthamoebic fungal Exposure Photokeratitis Cornealulcer Thygeson'ssuperficialpunctatekeratopathy Cornealdystrophy Fuchs' Meesmann Cornealectasia Keratoconus Pellucidmarginaldegeneration Keratoglobus 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Myopia Astigmatism Anisometropia /Aniseikonia Presbyopia VisiondisordersBlindness Amblyopia Leber'scongenitalamaurosis Diplopia Scotoma Colorblindness Achromatopsia Dichromacy Monochromacy Nyctalopia Oguchidisease Blindness /Visionloss /Visualimpairment Anopsia Hemianopsia binasal bitemporal homonymous Quadrantanopia subjective Asthenopia Hemeralopia Photophobia Scintillatingscotoma Pupil Anisocoria ArgyllRobertsonpupil MarcusGunnpupil Adiesyndrome Miosis Mydriasis Cycloplegia Parinaud'ssyndrome Other Nystagmus Childhoodblindness Infections Trachoma Onchocerciasis AuthoritycontrolNationallibraries Spain France(data) Germany Israel UnitedStates Japan Croatia 2 Other FacetedApplicationofSubjectTerminology SUDOC(France) 1 Retrievedfrom"https://en.wikipedia.org/w/index.php?title=Glaucoma&oldid=1097123260" 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