Glaucoma history and risk factors. Review

www.journalofoptometry.org

REVIEW

Glaucoma history and risk factors

Charles W. McMonnies

SchoolofOptometryandVisionScience,UniversityofNewSouthWales,Kensington2052,Australia

Received4December2015;accepted15February2016 Availableonline23March2016

KEYWORDS Glaucoma;

History;

Riskfactors;

Diagnosis

Abstract Apart from the risk of developing glaucoma thereis also the risk that it is not detected andirreversibleloss ofvision ensues.Some studiesofmethods ofglaucomadiag- nosishaveexaminedtheresultsofinstrument-basedexaminationswithgreatifnotcomplete relianceonobjectivefindings inarrivingatadiagnosis.The veryvaluableadvancesinglau- comadetectioninstrumenttechnologies,andapparentincreasingdependenceonthem,may haveledtoreducedconsiderationofinformationavailablefromapatienthistoryinthosestud- ies.Dependenceonobjectiveevidenceofglaucomatouspathologymayreducethepossibility ofdetecting glaucomasuspectsorpatients atrisk for becomingglaucoma suspects.A valid positivefamilyhistoryofglaucomaisveryvaluableinformation.However,negativefamilyhis- toriescanoftenbeunreliableduetolargenumbersofglaucomacasesbeingundiagnosed.No evidenceoffamilyhistoryisappropriateratherthannofamilyhistory.Inadditiontheunrelia- bilityofanegativefamilyhistoryisincreasedwhenpatientswithglaucomafailtoinformtheir familymembers.Afindingofnofamilyhistorycanonlybestatedasnoknownfamilyhistory.

Inexaminingthepotentialdiagnosticcontributionfromapatienthistory,thisreviewconsid- ers,age,frailty,race,typeanddegreeofrefractiveerror,systemichyper-andhypotension, vasospasm,migraine,pigmentarydispersionsyndrome,pseudoexfoliationsyndrome,obstruc- tivesleepapneasyndrome,diabetes,medicationinteractionsandsideeffects,thedegreeof exposure to intraocularandintracranial pressureelevations andfluctuations, smoking,and symptomsinadditiontogeneticsandfamilyhistoryofthedisease.

©2016SpanishGeneralCouncilofOptometry.PublishedbyElsevierEspa˜na,S.L.U.Thisisan openaccessarticleundertheCCBY-NC-NDlicense(http://creativecommons.org/licenses/by- nc-nd/4.0/).

PALABRASCLAVE Glaucoma;

Historial;

Factoresderiesgo;

Diagnóstico

Historialdeglaucomayfactoresderiesgo

Resumen Apartedelriesgodedesarrollarglaucoma,existetambiénelriesgodenodetec- tarlo,conlaconsiguientepérdidadevisiónirreversiblequeentra˜na.Algunosestudiossobrelos métodosparadiagnosticarelglaucomahanexaminadolosresultadosdelosexámenesbasados

∗Correspondenceto:CliffAvenue,Northbridge2063,Australia.Tel.:+61299583046;fax:+61299583012;mobile:+610409038799.

E-mailaddress:c.mcmonnies@unsw.edu.au

http://dx.doi.org/10.1016/j.optom.2016.02.003

1888-4296/©2016SpanishGeneralCouncilofOptometry.PublishedbyElsevierEspa˜na,S.L.U.ThisisanopenaccessarticleundertheCC BY-NC-NDlicense(http://creativecommons.org/licenses/by-nc-nd/4.0/).

eninstrumentos,quedependencasitotalmentedeloshallazgosobjetivosparalograrundiag- nóstico.Losmuyvaliososavancesenlatecnologíainstrumentalparaladeteccióndelglaucoma, yelincrementoaparentedeladependenciadedichosinstrumentos,puedenhaberllevadoa reducirlaconsideracióndelainformacióndisponibleenlahistoriadelpacienteendichosestu- dios.Ladependenciadelaevidenciaobjetivadelapatologíaglaucomatosapuedereducirla posibilidaddedetectarloscasosdesospechadeglaucoma,olospacientesconriesgodepasara lacategoríadesospecha,loquepuedemejorarlosresultadosdelasupervisióndeloscandidatos acirugíarefractiva.Unhistorialfamiliardeglaucomapositivoyválidoconstituyeunainforma- ciónmuyvaliosa.Sinembargo,loshistorialesfamiliaresnegativospuedenresultarpocofiables, debidoalgrannúmerodecasosdeglaucomasindiagnosticar.Lafaltadeevidenciadehistorial familiaresmásapropiadaquelaausenciadehistorialfamiliar.Además,lapocafiabilidaddelos historialesfamiliaresnegativosseincrementacuandolospacientesconglaucomanoinforman alosmiembrosdesufamilia.Unhallazgodeausenciadehistorialfamiliarpuedeestablecerse únicamentecomohistorialfamiliardesconocido.Alexaminarlapotencialcontribucióndiagnós- ticadelahistoriadelpaciente,estarevisiónconsideralaedad,lafragilidad,laraza,eltipoy gradodeerrorrefractivo,lahipertensiónehipotensiónsistémicas,elvasoespasmo,lamigra˜na, elsíndromededispersiónpigmentaria,elsíndromedepseudo-exfoliación,elsíndromedeapnea obstructivadelsue˜no,ladiabetes,lasinteraccionesmedicamentosasylosefectossecundarios, elgradodeexposiciónalaumentodelapresiónintraoculareintracraneal,eltabaquismo,ylos síntomas,ademásdelosfactoresgenéticosyelhistorialfamiliardelaenfermedad.

©2016SpanishGeneralCouncilofOptometry.PublicadoporElsevierEspa˜na,S.L.U.Esteesun art´ıculoOpenAccessbajolalicenciaCCBY-NC-ND(http://creativecommons.org/licenses/by- nc-nd/4.0/).

Glaucomainvolvesaprogressivelossofretinalganglion cells(RGC) andcharacteristicchanges inneuroretinalrim tissueintheopticnervehead(ONH)whichareaccompanied by visual field(VF) constriction.¹ There areseveral types ofglaucomaconstitutingagroupofeyediseaseswhichare theleadingcauseofirreversibleblindnessworldwide.²Apart fromtheriskofdevelopingglaucomathereistheriskthat itisnotdetectedandirreversiblelossofvisionensues.¹In asampleof5000urbanGreekpeopleover59yearsofage, 57.1%ofglaucomacaseswerefoundtobeundiagnosed.³A studyof3654predominantly whiteAustralians(90.2%over 60yearsof age and24% over80 yearsof age)found that theprevalenceofPOAGwas3.0%with51%nothavingbeen previouslydiagnosed.⁴Thatsomanycasesofglaucomacan be undiagnosed means that studies based in hospitals or specialist clinics, for example, can be biased to particu- lar classes of referred patients and sonot representative oftheGlaucomacohort⁵whichshouldideallyincludeallthe undiagnosedcases.Identificationoftheriskfactorsforglau- comadevelopmentrequirespopulation-basedstudies.⁵The prevalenceorincidenceofglaucomainapopulationstudy willdependonthethoroughnessoftheexaminationregime employed.

Comprehensivehistoryfindingsmaymakeanimportant contributiontothevaluableidentificationofglaucomasus- pectspriortoanyevidenceofglaucomatouschanges.Apart fromdiagnostic potential, decisions about treatment and follow-upschedulesmaybeimprovedbyreferencetohis- toryfindingsindicatingriskforandlikelyspeedofglaucoma progression for example. The findings of a thorough his- torymayaiddecisionsabouttherangeofobjectivetesting

requiredduringaclinicalexamination.Thepotentialforhis- torytocontributetodiagnosisandpatientmanagementmay becriticallymoreevidentwhenobjectivetestingindicates borderline or conflicting diagnostic findings. Screening of higher-riskgroupsmaybethemostcost-effectivemethodof reducingthevolumeofundiagnosedglaucoma⁶andpatient historyappearstobeapracticalmeansofscreeningtoiden- tifythehigherrisktargetpopulation.

Various combinations of patient history and objective methodsfortheevaluationoftheONH,retinalnervefibre layer (RNFL), VFs, tonometry, cornealthickness, tonogra- phy and provocative testing, for example, can be used toclassify subjects ashealthy, glaucoma suspects or hav- ingglaucomatouspathology.Apatient’sfamilyhistorymay improvetheaccuracyofglaucomapatientdiagnosticclas- sification in population studies as well as diagnosis in a clinical setting.⁷ In a general medical outpatient setting, a correct diagnosis was found to be determinedin 82.5%

of cases based onthe information providedby a medical history.⁸ There is a wide range of supplementary infor- mation in a patient history which may improve glaucoma diagnosis and treatment decisions. However, except for patient age in some cases, the findings of a patient his- tory may not be included in glaucoma studies.^9---13 Some studies may include the use of only familyhistory rather thanafullpatienthistory.^14---16Otherstudiesmaybelimited to objectivefindings from instrument-based examinations withrelianceonobjectivefindingstodeterminediagnostic classifications without reference to history or other clini- cal findings. For example, accuracy of diagnosis of early glaucoma wasfound to be greatest (although not always

significantly so) for ocular coherence tomography (OCT) RNFLthicknessparameters,followedbyFrequency-Doubling TechnologyVFanomalies,ScanningLaserPolarimetryRNFL anomalies, and lastly Short-Wavelength Automated Peri- metricVFanomalies.⁹ However,dependenceonsignificant evidenceof glaucomatouspathology reducesthe capacity to detect glaucoma suspects. The emphasis on the very valuable advances in the technology of glaucoma detec- tioninstruments,andassociatedincreasingapplicationsfor them,couldleadtoreducedattentionbeinggiventoinfor- mationavailablefromapatienthistory.Inastudyby Miki andcoauthorsglaucomasuspectsweredefinedasthosehav- ingglaucomatousopticneuropathy,orsuspicious-appearing opticdiscsbasedonstereophotographreviewbytwoexperi- encedgraders,orocularhypertension(intraocularpressure (IOP)>21mmHgatbaselinewithoutevidenceofrepeatable glaucomatousvisual fielddefect(VFD) at baseline.¹⁷ That study found that the rate of RNFL loss over timemay be a useful tooltohelp identifypatients whoareat risk for developingVFloss.¹⁷Suchresultsmaybeinterpretedasindi- catingthatOCTaloneisasuitablemethodofexamination.

However,notwithstandingtheusefulnessofthesefindings, thequestionremainsastowhetheracomprehensivepatient historycouldhaveidentifiedmoresubjectsatriskforhav- ing reduced RNFL thickness and VF loss. Case detection canbeimprovedbycombiningRNFLthicknessanalysiswith visualfunctiontests.¹⁸Howeverthisreviewre-evaluatesthe potentialforpatienthistorytoalsocontributetothediag- nosisofglaucomaandglaucomasuspects.Thedetectionof glaucomasuspectsdependsonpatienthistorywhenthereis nodetectableobjectiveevidenceofglaucoma.

Increasedmonitoring ofglaucoma patientsreduces the riskof undetectedprogression.¹⁹ Use ofdynamic andper- sonalised testing schedules can enhance the efficiency of detecting open-angle glaucoma (OAG) progression and reduce diagnostic delay compared withfixed yearly mon- itoring intervals.¹⁹ Ideally, monitoring schedules could be determinedaccordingtoindividualriskofdevelopingorpro- gressingglaucoma.Theperformanceofaforecastingmodel mightbeimprovedbyconsiderationofanysignificantfactors revealed by patient history. This review examines history detailswhichmayhelpdeterminediagnosticclassifications aswellashelpdetermineindividualtreatmentandfollow- upschedulesaccording totherisk andanticipatedrateof subsequentprogression.PubMedsearchesfor‘glaucomasus- pects’and‘glaucomaexamination’aswellasfor‘glaucoma suspects’and‘glaucomadiagnosis’yielded119and500ref- erences respectively. The most relevant of these to this reviewhavebeencited.

Age and frailty

Glaucomarisk increaseswith age.^20---22 As a consequence, glaucomacanbeexpectedtobeassociatedwithotherage- relateddiseases such asmacular degeneration,²⁰ vascular diseases,²³andobstructivesleepapnea²⁴forexample.How- everthisisnotadirectlinkformostage-relateddiseases.

Theconceptoffrailtyisanon-specificstate ofvulnerabil- ity which results in a higherrisk for accelerated physical andcognitivedecline,disabilityanddeath.²⁵Assessmentof frailtydependsontheaccumulationofhealthdeficits²⁶such

ashypertension,hypotension,diabetes,migraine,obstruc- tive sleep apnea syndrome, cataracts, glaucoma and the need for medications.²⁷ As is the case for glaucoma, the prevalenceofmanyotherhealthproblemstendstoincrease withfrailtyandmaybeanimportantreasonfortheirconcur- renceinsomepatients.Afrailpatientatayoungeragemay havegreaterriskfordevelopingglaucoma.

Gender

In the Ocular Hypertension Treatment (OHT) study, male gender was found by univariate analysis to be a useful predictor for the onset of primary open angle glaucoma (POAG).²⁸ A Bayesian meta-analysis found that men were more likely to have OAG with the reservation that gen- derinfluencedependsonthedefinitionofglaucoma.²⁹ For example,areviewoftheliteratureconcludedthatwomen areathigherriskforangle-closureglaucoma(ACG)butthat thereisnocleargenderpredilectionforOAG.³⁰Thesefind- ingsmayonlyberelevanttothegroupsstudied.Thatwomen usuallylivelongerthanmenincreasestheirriskforglaucoma andglaucomablindness.²⁹

Genetics and family history

Evidence of the significance of Myocilin mutations in advancedprimaryopenangle glaucoma(POAG)³¹ andcopy number variations of TBK1 in normal tension glaucoma (NTG)³² illustratethediagnosticpotentialforgenetictest- ing.However,thecontributionofgeneticsinglaucomarisk predictionhasusuallybeenlimitedtoknowledgeoffamily history³³although,toooften,patientsareunawareoffamily memberswhohavebeen diagnosedwithglaucoma.³⁴ That morethan50%ofglaucomacasescanbeundiagnosed³adds totheunreliabilityoffamilyhistory.Afamilyhistoryofglau- comawasfoundtocarryarelativeriskof2.1timesforbeing associatedwithatleastpossibleOAG²⁰ However,therela- tiveimportanceoffamilyhistorymayvaryaccordingtothe closenessofrelationshipofapatienttoanaffectedfamily member(first.secondoreventhirddegree).³⁵ Aroundhalf ofallprimaryOAG patientshaveapositivefamilyhistory, andtheirfirstdegreerelatives(parents,siblingsorchildren) havean approximately9-foldincreasedriskof developing glaucoma.³²Wolfsandco-authorsfoundthatthefirstdegree relativesofglaucomapatientswerefoundtohavea22%life- timeriskofglaucomathemselvesincomparisonto2.3%in relativesofnormalcontrols.³⁶ Theprevalenceofglaucoma was10.4%inthesiblingsofglaucomapatientscomparedto 0.7%inthesiblingsofnormalcontrols.³⁶Inaddition,therisk ofinheritingglaucomamayincreasewiththenumberofrel- ativesdiagnosedwiththedisease.Approximately60%ofa glaucomapatientsamplewasfoundtobelongtofamiliesin whichothermembershavethedisease.⁷

Race

Areview ofthe findingsfrom11population-based studies found a wide range in the prevalence of POAG among populations of the ‘‘same race’’.³⁷ Variable prevalence reportedindifferentstudiesmayhavebeenduetodifferent methodsofexaminationaswellasbeingaconsequenceof

differencesin exposuretogeographic,social, behavioural andenvironmentalfactors.³⁷ForcertainagegroupsRacette andco-authorsestimatedtheprevalenceofPOAGinablack American population, to be six times higher compared to whites.³⁸ Although black populations have the highest prevalenceofOAG,whitepopulationsshowedthesteepest increaseinOAGprevalencewithage.²⁹ Ahigherglaucoma prevalencehasbeenfoundinAsianpopulationsincludinga higherincidenceofprimaryangle-closureglaucoma(ACG) comparedtowhitepatients.³⁹

Myopia

Myopia has been found to be a significant risk factor for glaucoma.^21,39---44Thatmyopiaisariskfactor forglaucoma andthatitisalsomoreprevalentamongAsianpatientsmay helpexplainincreasedprevalence.³⁹ Inaddition,thathigh myopia⁴² andincreasedaxial lengthin certainage groups haveboth been identifiedasrisk factors^43,44 suggeststhat theriskofglaucomadevelopmentandprogressionincreases withthedegreeofmyopia.⁴⁴

The type of glaucoma may vary with refractive error

Thesignificanceofhistoryitemsmayvarywiththetypeof glaucoma.Forexample,riskfactorsforacuteACGinclude hyperopia⁴⁵andmyopiaisasignificanthistoryitemforpro- gressionofocularhypertension(OHT)andPOAG.⁴⁰

Systemic hypotension and hypertension

Systemichypertension,vasospasm,and acutehypotension havebeen proposedaspotentialrisk factorsforglaucoma in clinic-based studies.^46---48 Several studies have reported associations between low diastolic pressure, lower ocu- larperfusionpressure(OPP)andhigherprevalenceand/or incidence of glaucoma.^46---49 Low systemic blood pressure (BP),especiallywhen combinedwithanelevated IOP,will lower OPP and risk a reduction in the volume of blood flowtotheONH in eyeswithanimpaired auto-regulatory system,⁵⁰ leading to ischaemic and reperfusion oxidative stressdamagetothe axonsandassociatedatrophy ofthe RGCs.A historyofantihypertensive treatmentand associ- atedlowerBP couldincreasetherisk ofglaucoma bythis mechanism.⁵¹ The Blue Mountains population study found thatmeanIOPincreasedlinearlyfrom14.3mmHgforsystolic BP<110mmHgto17.7mmHgforsystolicBP>200mmHg.⁵²A study of 4297 subjects over 40 years of age in a defined predominantly white population found a positive corre- lation between systemic BP and IOP and an association between POAG and systemic hypertension.⁴⁷ However, a cross-sectionalpopulationstudyconcludedthattheassoci- ationbetweenhypertensionandPOAGwasmostlikelydue tothecorrelationbetweenageandhypertension.²¹

Vasospasm

Vasospasm represents vascular dysregulation associated withinappropriateconstrictionor insufficientdilatationin

themicrocirculation.⁵³ Theeye isfrequentlyinvolved ina vasospasticsyndromewithvasospasmassociatedwithante- riorischaemicopticneuropathyandglaucoma.⁵³Vasospasm is often falsely equated with Raynaud’s phenomenon.⁵³ Vasospasmpatientsoftenpresentwithcoldhandsymptoms but they usually do not have the pale fingers which are characteristic of Raynaud’s disease.⁵³ Vasospasm patients frequentlyhavelowBP⁵³ which,asdiscussed,mayalsobe associatedwithreducedOPPandglaucomarisk.

Migraine

An association between NTG and migraine has been sug- gested, with a potential common vascular aetiology for bothdiseases.⁵⁴ However,anassociationbetweenOAGand migrainewasfoundtoonlybesignificantforsubjectsaged 70---79years.⁵⁵

Pigmentary dispersion syndrome

Pigmentary glaucoma characteristically developsin young myopic patients with pigmentary dispersion syndrome.⁵⁶ Male gender, black race, severe myopia, and Krukenberg spindleswereidentifiedaspossibleriskfactorsforthedevel- opmentandseverityofglaucomainthepigmentdispersion syndrome.⁵⁷

Pseudoexfoliation syndrome

Pseudoexfoliationsyndromeis acommonage-relatedgen- eralisedfibroticmatrixprocess⁵⁸withsignificancebecause itincreasestheriskofdevelopingglaucoma.^20,22

Obstructive sleep apnea syndrome

Comparedtonormalpatients,obstructivesleepapneasyn- drome patients were found to have 1.67 times greater likelihoodof developingglaucomaover a5year follow-up period.²⁴

Diabetes

Ameta-analysisbyZhouandco-authorsfoundthatsixcase- controlstudiesindicateddiabetesasariskfactorforPOAG withameanoddsratiogreaterthanone,while aseventh study found an odds ratio of 0.61.⁵⁹ Of six population- basedcohortstudiesfiveindicatedasignificantassociation between diabetes mellitus and POAG.⁵² It appears that diabetesmayincreasetheriskofPOAG,especiallyashyper- glycaemiaresultsinheightenedsensitivitytoIOPandriskof neuronalinjury.⁵³ When 80NTG and4015control patients were compared in a Korean population, a higher propor- tionoffastingcapillaryglucose≥200mg/dLwasidentified asariskfactorforOAGinbothunivariateandmultivariate analyses.³⁵ Nevertheless,theassociationbetweendiabetes andglaucomaremainscontroversial.⁶⁰

Medication-related IOP elevation

Theconcomitantuseofglaucomaandsystemicmedications forco-existingsystemicdisorderscreatesthepotentialfor druginteractions,aswellassideeffectsfrombothgroups of drugs.⁶¹ For example,ACG due to pupillary block, can becausedbylocalorsystemicadministrationofadrenergic agents, as well as by sulfa-based drugs⁶² Corticosteroid- induced glaucoma and OHT is a response to increased resistance to aqueous outflow.⁶³ Treatment for systemic hypertension or Raynaud’s diseasecould increase therisk ofglaucoma.⁵¹ Forexample,a fiveyear follow-upof3271 subjectsfoundtheriskfactorsassociatedwiththeincidence ofPOAGdevelopmentincludedhavingevertakencalcium- channel or alpha-blockermedication.²⁰ However, whether alpha-blockingmedicationshave anyhaemodynamic influ- enceontheONHremainstobeelucidated.²⁰

Smoking

Studies of the association between glaucoma and smok- ing have been contradictory.⁶⁰ It has been hypothesised that, in thepresence of genetic risk factors,exposure to environmentalstressessuchassmoking,corticosteroidmed- ication anddiabetes, results inan earlier ageof onsetof glaucoma.⁶⁰Theriskofglaucomainsmokersmaybehigher inmen.⁶⁰

Exposure to IOP elevation and fluctuation

IOP is the only knownmodifiable factor in OAG.¹² Oneof thefactorsassociatedwithprogressionofglaucomaisfluc- tuationinIOPeitheroverthe24hdiurnalperiodor across visits.^64---67 Forexample,inNTGpatient’sprogressionofVF losseswasfound tobe associatedwithahigher24h peak IOP and greater IOP fluctuation over 24h.⁶⁸ Exposure to IOP elevationsand fluctuationswhich occurduring avari- ety of regular or occasional activities may increase the risk for the development or progressionof glaucoma.^69---71 For example activities involving sleep-related postures,⁷¹ lidsqueezing/squinting,eyewiping,massagingorrubbing, inverted body positions (suchas inthe practice of Yoga), wearingswimminggoggles,musculareffort,increasedexpi- ratory effort such as during physical exercise or when playinghighwindresistantmusicalinstruments,andwear- ing a shirt or tie which are tight around the neck are allknowntoelevateIOP,⁶⁷ sometimesin conjunctionwith intracranialpressureelevation.⁷² Reducingparticipationin activitieswhichelevateeitherorbothIOPandintracranial pressurewilldecreaseexposuretohigherlevelsoflamina cribrosadisplacement and/orlamina cribrosacompression withthe associated possibility of risk of damage toRNFL axons passing through the lamina cribrosa.⁷² Although a single short-term fluctuation is likely to be of negligible significance,thecumulativeeffectofconstantorfrequent fluctuationcouldbesignificantincontributingtoglaucoma pathogenesis.⁷³ Any risk associated with a single short- termfluctuationmayincreasewiththedegreeofelevation involved.IOPmeasuredwiththepatientsittingwithneckin aneutralposition(noflexionor extension)isprobablythe lowestofanybodyposition.⁷⁴ Estimationofthedegreeof

exposuretoIOP elevationandfluctuationepisodes,some- timestolevelsmanytimesthesitting-positionlevel,canbe aidedbyquestionnaireresponses.⁶⁷(Copiesofthequestion- nairecanbeobtainedfromc.mcmonnies@unsw.edu.au.)

Symptoms

Glaucomaprogression carries a burden of both nonvisual andvisual symptomswhich areaconsiderable concern to patients in more advanced cases.⁷⁵ However,at the time ofdiagnosis,mostpatientsarerelativelyfreeofglaucoma- inducedimpairments.⁷⁶Theabsenceofsymptomswhichare specificto early glaucoma appearslikely tocontribute to the high number of undiagnosed subjects found in popu- lationstudies.^75,76 The GlaucomaSymptom Scale provides avalidandreliableestimateofsymptomsassociatedwith glaucomaanditstreatments.⁷⁵However,fortheearlystages ofglaucoma,sensitivitymaybehighandspecificitycorre- spondinglylow withthis instrument becausemany of the GlaucomaScalesymptomssuchasburning,smarting,sting- ing,tearing,dryness,itching,sorenessandtiredness⁷⁵ can occur in many diseases such as any of the dry eye syn- dromes,andeveninotherwisehealthyeyesduringexposure toadverseenvironmentalconditions.However,thesetypes ofsymptomsmayoccurasaconsequenceofglaucomatreat- ment.Inbothclinicalandresearchsettingsthisscaleshould provetobeavaluablepatient-centredtoolfortheassess- mentandcomparisonofsymptomsexperiencedbypatients withglaucomaespeciallyperhapsforthosewhopresentwith newsymptomswhileundergoingtreatment.⁷⁵

Discussion

Comprehensive history findings may make an important contributiontotheidentificationofglaucomasuspectsprior toany evidenceof glaucomatouschanges.The findingsof a thorough history may aid decisions about the range of objective testing required during a clinical examination.

The potential value for a comprehensive history in deci- sionmakingmaybegreaterwhenobjectivetestingindicates borderline or conflictingdiagnostic findings.Forexample, OCTusingguided progressionanalysissoftware,perimetry and stereophotography examinations were repeated dur- ingfollow-up toexamine for glaucomatous progressionin 246eyes.¹³ Notwithstandingsomeagreementbetweenthe threemethods,most cases withdetectable changeswere identified by only one of these methods of examination.

These findings suggest that reference to history informa- tionmayassistdecisionmakingwhenglaucomamonitoring examination findings obtained with different instruments arenotinagreementorareataborderlinelevelinregard torecommended diagnostic cut-offs for particular instru- ments.Itisimportanttostressthatapredictiveinstrument suchasacomprehensivehistory¹⁵aswellasaninstrument- based objective predictive risk model should always be supplementedbyclinicaljudgement.¹²Theneedforclinical judgementmaybereducedifit waspossibletoappropri- atelyweightthesignificanceof individualhistoryitemsin relationtoglaucoma diagnosisinorderthatthecombined predictive performance of a history could be maximised.

Combining multiple-screening strategies together with

family history can be a very powerful diagnostic method forglaucoma.¹⁵ Noevidenceof afamilyhistorycanbean appropriatefindingwhereasa findingof nofamilyhistory cannot be made confidently. However, given itspotential for unreliability, rather than considering only the pres- enceof a familyhistory ofglaucoma, the combination of acomprehensive historyand clinicalassessment²⁰ maybe moresuccessful,especiallyinmarginal/suspectdiagnoses.

Geneticvariations relatedtoOAG may provide additional indicationofrisk.⁷⁷ Apartfromdiagnosticpotential,treat- mentandtheappropriateness offollow-up schedulesmay beimprovedbyreferencetohistoryfindings.Forexample, apatient’shistorymayalsocontributetodifficultmanage- mentdecisionsincasesofocularhypertension.Screeningof higher-riskgroupsmaybethemostcost-effectivemethodof reducingthevolumeofundiagnosedglaucoma⁷⁸andpatient historyappearstobeapracticalmeansofhelpingtoiden- tifypatientswithhigherriskfordevelopingglaucoma.Asa possibleconsequence of the importanceplaced onobjec- tivefindings in recent literature,the potentialusefulness of history findings may sometimes be ignored or under- emphasised.

Funding

Therearenofunding,proprietary orfinancial intereststo declareinrelationtothispaper.

References

1.ShonK,WollsteinG,SchumanJS,SungKR.Predictionofglau- comatousfieldprogression:pointwiseanalysis.CurrEyeRes.

2014;39:705---710.

2.Quigley HA, Broman AT. The number of people with glau- coma world wide in 2010 and 2020. Br J Ophthalmol.

2006;90:262---267.

3.TopouzisF,ColemanAL,HarrisA,etal.Factorsassociatedwith undiagnosedopen-angleglaucoma:theThessalonikiEyeStudy.

AmJOphthalmol.2008;145:327---335.

4.Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia. Ophthalmology.

1996;103:1661---1669.

5.TatemichiM,NakanoT, TanakaK, etal.Possibleassociation betweenheavycomputerusersandglaucomatousvisualfield abnormalities:acrosssectionalstudyinJapaneseworkers.J EpidemiolCommunityHealth.2004;58:1021---1027.

6.MaulEA,JampelHD.Glaucomascreeningintherealworld.

Ophthalmology.2010;117:1665---1666.

7.GreenMG,KearnsLS,WuJ,etal.Howsignificantisafamily history of glaucoma. Experience from the Glaucoma Inher- itance Study in Tasmania. Clin Exp Ophthalmol. 2007;35:

793---799.

8.Hampton JR, Harrison MJG,Mitchell JRA, Prichard JS, Sey- mour C. Relative contributions of history-taking, physical examination, and laboratory investigation to diagnosis and management of medical outpatients. Br J Med. 1975;2:

486---489.

9.BowdC,ZangwillLM,BerryCC,etal.Detectingearlyglaucoma byassessmentofretinalnervefiberlayerthicknessandvisual function.InvestOphthalmolVisSci.2001;42:1992---2003.

10.FosterPJ,BuhrmannQuigleyHA,JohnsonGJ.Thedefinition andclassificationofglaucomainprevalencesurveys.BrJOph- thalmol.2002;86:238---242.

11.Huang ML, Chen HY. Development and comparison of automated classifiers for glaucoma diagnosis using Stratus opticl coherence tomography. Invest Ophthalmol Vis Sci.

2005;46:4121---4129.

12.Gordon MO, Torri V, Miglior S, et al. Validated prediction model for the development of primary open-angle glau- comainindividualswithocularhypertension.Ophthalmology.

2007;114:10---19.

13.Banegas SA, Anton A, Bogado M, Ayala EM. Agreement among spectral-domain opical coherence tomography, stan- dard automated perimetry, and stereophotography in the detectionofglaucomaprotection.InvestOphthalmolVisSci.

2015;56:1253---1260.

14.Robin TA, Muller A, Rait J, Keefe JE, Taylor HR, Mukesh BN.Perforanceofcommunity-basedglaucomascreeningusing FrequencyDoublingTechnologyandHeidelbergRetinaltomog- raphy.OphthalmicEpidemiol.2005;12:167---178.

15.Saito H, Tsutsumi T, Araie M, Tomidokoro A, Iwase A.

Glaucoma screening in the real world. Ophthalmology.

2011;118:1008---1009.

16.HealeyPR,MitchellP.Glaucomascreeningintherealworld.

Ophthalmology.2011;118:1009.

17.MikiA,MedeirosFA,WeinrebRN,etal.Ratesofretinalnerve fiberlayerthinninginglaucomasuspecteyes.Ophthalmology.

2014;121:1350---1358.

18.Dabasia PL, Fidalgo BR, Edgar DF, Garway-Heath DF, LawrensonJG.Diagnosticaccuracyoftechnologiesfor glau- coma case-finding in a community setting. Ophthalmology.

2015;122:2407---2415.

19.Schell GJ, Lavieri MS, Helm JE, et al. Usingfiltered fore- casting techniques to determine personalized monitoring schedulesforpatientswithopen-angleglaucoma.Ophthalmol- ogy.2014;121:1539---1546.

20.LeA,MukeshBN,McCartyCA,TaylorHR.Riskfactorsassoci- atedwiththeincidence ofopen-angle glaucoma:thevisual impairment project. Invest Ophthalmol Vis Sci. 2003;44:

3783---3789.

21.SuzukiY,Iwase A,AraieM,et al.,TajimiStudyGroup.Risk factorsforopen-angleglaucomainaJapanesepopulation.The TajimiStudy.Ophthalmology.2006;113:1613---1617.

22.MigliorS,PfeifferN,TorriV,ZeyenT,Cunha-VazJ,Adamsons ItheEuropeanGlaucomaPreventionStudy(EGPS)Group.Pre- dictivefactorsforopen-angleglaucomaamongpatientswith ocular hypertension in the European Glaucoma Prevention Study.Ophthalmology.2007;114:3---9.

23.Nateras OSE, Harrison JM, Muir ER, et al. Choroidal blood flow decreases with age: an MRI study. Curr Eye Res.

2014;39:1059---1067.

24.Lin C-C, Hu C-C, Ho J-D, Chiu H-W, Lin H-C. Obstructive sleepapneaandincreasedriskofglaucoma.Ophthalmology.

2013;120:1559---1564.

25.FulopT,LarbiA,WitkowskiJM,etal.Aging,frailtyandage- relateddiseases.Biogerontology.2010;11:547---563.

26.RockwoodK, SongX, MitnitskiA. Changesinrelativefitness andfrailtyacrosstheadultlifespan:evidencefromtheCana- dian National Population Health Survey. Can Med Assoc J.

2011;183:E487---E494.

27.Song X, Mitnitski A, Rockwood K. Prevalence of 10 year outcomesoffrailtyinolderadultsinrelationtodeficitaccu- mulation.JAmGeriatSoc.2010;58:681---687.

28.GordonMO,BeiserJA, BrandtJD, etal. TheOcular Hyper- tension Treatment Study: baseline factors that predict the onset of primary open angle glaucoma. Arch Ophthalmol.

2002;120:714---720.

29.RudnickaAR,Mt-IsaS,OwenCG,CookDG,AshbyD.Variations inprimary open-angleglaucoma prevalencebyage,gender, andrace:aBayesianmeta-analysis.InvestOphthalmolVisSci.

2006;47:4254---4261.

30.VajaranantTS,NayakS, WilenskyJT,Joslin CE.Genderand glaucoma:whatweknowandwhatwedon’tknow.CurrOpin Ophthalmol.2010;21:91---99.

31.SouzeauE,BurdonKP,DubowskyA,etal.Higherprevalence ofmyocilin mutations inadvanced glaucoma in comparison withlessadvanceddiseaseinanAustralianDiseaseRegistry.

Ophthalmology.2013;120:1135---1143.

32.AwadallaMS,FingertJH,RoosBE,etal.Copynumbervaria- tionsofTBK1inAustralianpatientswithprimaryopen-angle glaucoma.AmJOphthamol.2015;159:124---130.

33.McNaught AL, Allen JG, Healey DL, et al. Accuracy and implicationsofa reportedfamily history ofglaucoma. Arch Ophthalmol.2000;118:900---904.

34.TaylorH.Glaucomascreeningintherealworld.Ophthalmol- ogy.2011;118:1008.

35.CongdonN, Wang F,Tielsch JM.Issuesin epidemiology and population-based screening of primary angle-closure glau- coma.SurvOphthalmol.1992;36:411---423.

36.WolfsRGC,KlaverCCW,RamrattanRS,VanDuijnCM,Hofman A,deJongPTVM.Geneticriskofprimaryopen-angleglaucoma.

ArchOphthalmol.1998;116:1640---1645.

37.Kosoko-LasakiO,GongG,HaynatskiG,RaceWilsonR.ethnicity andprevalenceofprimaryopen-angleglaucoma.JNationMed Assoc.2006;98:1626---1629.

38.RacetteL, WilsonMR,ZangwillLM,WeinrebRN,SamplePA.

Primaryopen-angle glaucomainblacks:a review.SurvOph- thalmol.2003;48:295---313.

39.ChoH-K,KeeC.Population-basedglaucomastudiesinAsians.

SurvOphthalmol.2014;59:434---447.

40.LanderJ,GoldbergI,GrahamSL.Analysisofriskfactorswhich may be associated with progression from ocular hyperten- siontoprimary open-angle glaucoma.Clin ExpOphthalmol.

2002;30:242---247.

41.Kim MJ, Kim JM, Kim HS, Jeoung JW, Park KH. Risk fac- torsforopen-angleglaucomawithnormalbaselineintraocular pressure in a young population:the Korea National Health and Nutrition Examination Survey. Clin Exp Ophthalmol.

2014;42:825---832.

42.YamamotoS,SawaguchiS,IwaseA,etal.Primaryopen-angle glaucoma in a population associated with high preva- lence of primary open-angle glaucoma. Ophthalmology.

2014;121:1558---1565.

43.VijayaL,RashimaA,PandayM,etal.Predictorsforincidence ofprimaryopen-angleglaucomainasouthIndianpopulation.

Ophthalmology.2014;121:1370---1376.

44.MarcusMW,deVriesMM,MontolioJ,JansoniusNM.Myopiaas ariskfactorforopen-angleglaucoma:asystematicreviewand meta-analysis.Ophthalmology.2011:1994---1998.

45.XuL,FangW,WangYX,ChenCX,JonasJB.Anteriorchamber depthandchamberangleandtheirassociationswithocularand generalparameters:theBeijingEyeStudy.AmJOphthalmol.

2008;145:929---936.

46.TopouzisF,ColemanAL,HarrisA,etal.Associationofblood pressurestatuswiththeopticdiskstructureinnon-glaucoma subjects: the Thessaloniki Eye Study. Am J Ophthalmol.

2006;142:60---67.

47.BonomiL,MarchiniG,MarraffaM,BernadiP,MorbioR,Varotto A.Vascularriskfactorsforopen-angleglaucoma.Ophthalmol- ogy.2000;107:1287---1293.

48.Leske MC, Wu S-Y, Hennis A, Honkanen R, Nemesure B, Barbados Eye Study Group. Risk factors for incident open- angleglaucoma: the BarbadosEye Studies. Ophthalmology.

2008;115:85---93.

49.ZhaoD,ChoJ,KimMH,GuallarE.Theassociationofblood pressureand primaryopen-angleglaucoma:ameta-analysis.

AmJOphthalmol.2014;158:615---627.

50.CostarVP,HarrisA,AndersonD,etal.Ocularperfusionpressure inglaucoma.ActaOphthamol.2014;92:e252---e266.

51.LeskeMC.Theepidemiologyofopen-angleglaucoma:areview.

AmJEpidemiol.1983;118:166---186.

52.MitchellP,LeeAJ,WangJJ,RochtchinaE.Intraocularpressure overtheclinicalrangeofbloodpressure:BlueMountainsEye Studyfindings.AmJOphthalmol.2005;140:131---132.

53.FlammerJ,PacheM,ResinkT.Vasospasm,itsroleinthepatho- genesisofdiseaseswithparticularreferencetotheeye.Prog RetEyeRes.2001;20:319---349.

54.Cursiefen C, Wisse M, Cursiefen S, Junemann A, MartusP, Korth M. Migraine and tension headache in high-pressure andnormal-pressureglaucoma.AmJOphthalmol.2000;129:

102---104.

55.WangJJ,MitchellP,SmithW.Isthereanassociationbetween migraine headachesand open-angle glaucoma. Ophthalmol- ogy.1997;104:1714---1719.

56.Siddiqui Y,Ten HulzenRD,Cameron JD, HodgeDO,Johnson DH. What is the risk of developing pigmentary glau- comafrompigmentdispersionsyndrome.AmJOphthalmol.

2003;135:794---799.

57.Farrar SM, Shields MB, Miller KN, Stoup CM. Risk factors for the development and severity of glaucoma in the pig- ment dispersion syndrome. Am J Ophthalmol. 1989;108:

223---229.

58.Schlotzer-Schrehardt U, Naumann OH. Ocular and sys- temic pseudoexfoliation syndrome. Am J Ophthalmol.

2006;141:921---937.

59.ZhouM,Wang W,HuangW, ZhangX.Diabetes mellitusasa riskfactorforopen-angleglaucoma:asystematicreviewand meta-analysis.PLoSONE.2014;9.

60.DoucetteLP,RasnitsynA,SeifiM,WalterMA.Theinteractions ofgenes,age,andenvironmentinglaucomapathogenesis.Surv Ophthalmol.2015.

61.GottfredsdottirMS,AllinghamRR,ShieldsBM.Physicians’guide tointeractionsbetweenglaucomaandsystemicmedications.

JGlauc.1997;6:377---383.

62.LachkarY,BouassidaW.Drug-inducedacuteangleclosureglau- coma.CurrOpinOphthalmol.2007;18:129---133.

63.JonesR3rd,RheeDJ.Corticosteroid-inducedocularhyperten- sionandglaucoma:abriefreviewandupdateoftheliterature.

CurrOpinOphthalmol.2006;17:163---167.

64.AsraniS,ZeimerR,WilenskyJ,GieserD,VitaleS,Lindenmuth K. Large diurnalfluctuations in intraocular pressure are an independentriskfactorinpatientswithglaucoma.JGlaucoma.

2000;9:134---142.

65.Varma R, Hwang L-J, Grunden JW, Bean GW. Inter-visit IOP range: an alternative parameter for assessing intraoc- ular pressure control in clinical trials. Am J Ophthalmol.

2008;145:336---342.

66.Mansouri K, Medeiros FA, Weinreb RN. 24-Hour versus day- time intraocular pressure phasing in the management of patientswithtreated glaucoma. BrJ Ophthalmol.2011;95:

594---595.

67.McMonniesCW.Anexaminationofthehypothesisthatintraocu- larpressureelevationepisodescanhaveprognosticsignificance inglaucomasuspects.JOptom.2014.

68.Sakata R, Aihara M, Murata H, et al. Intraocular pres- surechangesover ahabitual24-hourperiod,afterchanging posture or drinking water and related factors in nor- mal tension glaucoma. Invest Ophthalmol Vis Sci. 2013;54:

5313---5320.

69.McMonnies CW. Intraocular pressure spikes in keratecta- sia, axial myopia and glaucoma. Optom Vis Sc. 2008;85:

1018---1026.

70.McMonniesCW.Intraocularpressureandglaucoma:isphysical exercisebeneficialorarisk?JOptom.2015.

71.McMonnies CW. The significance of intraocular pressure elevation during sleep-related postures. Clin Exp Optom.

2014;97:221---224.

72.McMonniesCW.Theinteractionbetweenintracranialpressure, intraocularpressureandlaminacribrosacompressioninglau- coma.ClinExpOptom.2015[inpress].

73.Gardiner SK,Johnson CA,DemirelS. Factorspredicting the rateoffunctionalprogressioninearlyandsuspectedglaucoma.

InvestOphthalmolVisSci.2012;53:3598---3604.

74.SitAJ.Intraocularpressurevariations;causesandclinicalsig- nificance.CanJOphthalmol.2014;49:484---488.

75.LeeBL,GutierrezP,GordonM,etal.Theglaucomasymptom scale.ArchOphthalmol.1998;116:861---866.

76.MillsRP.Correlationofqualityoflifewithclinicalsymptoms andsignsatthetimeofglaucomadiagnosis.TransAmOph- thalmolSoc.1998;96:753---812.

77.BurdonKP,MitchellP,LeeA,etal.Associationofopen-angle glaucomalociwithincidentglaucomaintheBlueMountains eyestudy.AmJOphthalmol.2015;159:31---36.

78.Burr JM, Mowatt G, Hernandez R, et al. The clinical per- formanceand cost-effectivenessofscreeningforopen-angle glaucoma: a systematic reviewand econonomicevaluation.

HealthTechnolAssess.2007;11.