• Nem Talált Eredményt

ADHD Updated European Consensus Statement on diagnosis and treatment ofadult European Psychiatry

N/A
N/A
Protected

Academic year: 2022

Ossza meg "ADHD Updated European Consensus Statement on diagnosis and treatment ofadult European Psychiatry"

Copied!
21
0
0

Teljes szövegt

(1)

Original article

Updated European Consensus Statement on diagnosis and treatment of adult ADHD

J.J.S. Kooij

a,b,

*, D. Bijlenga

a

, L. Salerno

9

, R. Jaeschke

1

, I. Bitter

J

, J. Balázs

c

,

J. Thome

S

, G. Dom

X

, S. Kasper

d

, C. Nunes Filipe

7

, S. Stes

e

, P. Mohr

W

, S. Leppämäki

f

, M. Casas

g

, J. Bobes

O

, J.M. Mccarthy

h

, V. Richarte

i

, A. Kjems Philipsen

j

, A. Pehlivanidis

8

, A. Niemela

k

, B. Styr

l

, B. Semerci

10

, B. Bolea-Alamanac

m

, D. Edvinsson

n

, D. Baeyens

o

, D. Wynchank

a

, E. Sobanski

L

, A. Philipsen

p

, F. McNicholas

4

, H. Caci

M

, I. Mihailescu

q

, I. Manor

3

, I. Dobrescu

r

, T. Saito

H

, J. Krause

5

, J. Fayyad

s

, J.A. Ramos-Quiroga

N

, K. Foeken

t

, F. Rad

u

, M. Adamou

v

, M. Ohlmeier

6

, M. Fitzgerald

w

, M. Gill

Q

, M. Lensing

U

,

N. Motavalli Mukaddes

x

, P. Brudkiewicz

y

, P. Gustafsson

11

, P. Tani

z

, P. Oswald

12

,

P.J. Carpentier

A

, P. De Rossi

Y

, R. Delorme

B

, S. Markovska Simoska

C

, S. Pallanti

D

, S. Young

E

, S. Bejerot

V

, T. Lehtonen

F

, J. Kustow

G

, U. Müller-Sedgwick

K

, T. Hirvikoski

Z

, V. Pironti

2

, Y. Ginsberg

T

, Z. Félegyházy

I

, M.P. Garcia-Portilla

R

, P. Asherson

P

aPsyQPsycho-MedicalPrograms,ExpertiseCenterAdultADHD,CarelReinierszkade197,2593HR,TheHague,TheNetherlands

bAmsterdamUMC,LocationVUMc,Dept.ofPsychiatry,Amsterdam,theNetherlands

cInstituteofPsychology,EotvosLorandUniversity,VadaskertChildPsychiatricHospialandOutpatientClinic,Budapest,Hungary

dMedicalUniversityVienna,DepartmentofPsychiatryandPsychotherapy,Vienna,Austria

eUniversityPsychiatricCenter,KULeuven,Kortenberg,Belgium

fHelsinkiUniversityCentralHospital,DepartmentofPsychiatry,HUS,Finland

gDepartmentofPsychiatry,HospitalUniversitariValld’Hebron,Barcelona,Catalonia,Spain;PsychiatricGeneticsUnit,Valld’HebronResearchInstitute (VHIR),Barcelona,Catalonia,Spain;BiomedicalNetworkResearchCentreonMentalHealth(CIBERSAM),Barcelona,Catalonia,Spain;Departmentof PsychiatryandForensicMedicine,UniversitatAutònomadeBarcelona,Barcelona,Catalonia,Spain

hVisitingseniorlecturer,King’sCollegeLondon,UnitedKingdom;MidlandRegionalForensicService,Hamilton,NewZealand

iDepartmentofPsychiatry,HospitalUniversitariValld’Hebron,Barcelona;BiomedicalNetworkResearchCentreonMentalHealth(CIBERSAM),Barcelona;

DepartmentofPsychiatryandLegalMedicine,UniversitatAutònomadeBarcelona,Barcelona,Spain

jDPCNaestved,Ladby,Naestved,RegionSjaelland,Denmark

kWellmindTerveysOy,Oulu,Finland

lMccabiHealthServices(H.M.O),TelAviv,Israel

mGeneralSystemsDivision,CentreforAddictionandMentalHealth/Dept.OfPsychiatry,UniversityofToronto,Toronto,Canada

nUppsalaUniversity,UppsalaUniversityHospital,Akademiskasjukhuset,Uppsala,Stockholm

oParentingandSpecialEducation,KULeuven,Leuven,Belgium

pUniversityofBonn,DepartmentofPsychiatryandPsychotherapy,Bonn,Germany

qAlexandruObregiaClinicalHospitalofPsychiatry,Bucharest,Romania

rUniversityofMedicineandPharmacy“CarolDavila”.ChildandadolescentPsychiatryDepartment,Prof.Dr.AlexObregia”PsychiatryHospital,Bucharest, Romania

sStGeorgeHospitalUniversityMedicalCenter,BalamandUniversityFacultyofMedicine,InstituteforDevelopment,Research,AdvocacyandAppliedCare, DepartmentofPsychiatryandClinicalPsychology,StGeorgeHospital,Achrafieh,Beirut,Lebanon

tVieuxChemindeCagnesàLaGaude,laGaude,France

uUniversityofMedicineandPharmacy“CarolDavila”;ChildandadolescentPsychiatryDepartment,Prof.Dr.AlexObregia”PsychiatryHospital,Bucharest, Romania

vUniversityofHuddersfieldandSouthWestYorkshirePartnershipNHS,ManygatesClinic,Wakefield,England

wTrinityCollege,BlanchardstownVillage,Dublin,RepublicofIreland

xIstanbulInstituteofChildandAdolescentPsychiatry,Istanbul,Turkey

yCentrumDobrejTerapii,Cracow,Poland

zDepartmentofPsychiatry,ClinicforNeuropsychiatry,HelsinkiUniversityCentralHospital,HUS,Finland

AReiniervanArkelMentalHealthInstitute,’s-Hertogenbosch,Netherlands

BChildandAdolescentPsychiatryDepartment,RobertDebréHospital,Paris,France

CMacedonianAcademyofSciencesandArts,Skopje,RepublicofMacedonia

DStanfordUniversityMedicalCenter,UniversityofFlorence,INSInstituteofNeuroscience,Florence,Italy

EPsychologyServicesLimited,Croydon,England

FNeuropsykologkonsultTainaLehtonen,Hjärup,Sweden

GBarnetAdultADHDService,Barnet,EnfieldandHaringeyNHSMentalHealthTrust,London;BarnetAdultADHDService,SpringwellCentre,BarnetHospital, Barnet,England

HDepartmentofChildandadolescentPsychiatry,GraduateSchoolofMedicine,HokkaidoUniversity,North15,West7,Kita-ku,Sapporo,060-8638Japan

http://dx.doi.org/10.1016/j.eurpsy.2018.11.001

0924-9338/©2018TheAuthor(s).PublishedbyElsevierMassonSAS.ThisisanopenaccessarticleundertheCCBY-NC-NDlicense(http://creativecommons.org/licenses/by- nc-nd/4.0/).

ContentslistsavailableatScienceDirect

European Psychiatry

j o u r n a l h o m e p a g e : h t tp : / / w w w . e u r o p s y - j o u r n al . c o m

(2)

IADHDKözpont(center)Budapest,Budapest,Hungary

JSemmelweisUniversity,DepartmentofPsychiatry,Budapest,Hungary

KAdultADHDService,Barnet,Enfield&HaringeyNHSMentalHealthTrust,NorthLondon&DepartmentofPsychiatry,UniversityofCambridge;AdultADHD Service,SpringwellCentre/BarnetHospital,Barnet,London,England

LCentralInstituteofMentalHealth,Mannheim;UniversityMedicalCenterMainz,Mainz,Germany

MHopitauxPediatriquesdeNiceCHULenval,Nice,France

NDepartmentofPsychiatry,HospitalUniversitariValld’Hebron,Barcelona,Catalonia,Spain;PsychiatricGeneticsUnit,Valld’HebronResearchInstitute (VHIR),Barcelona,Catalonia,Spain;BiomedicalNetworkResearchCentreonMentalHealth(CIBERSAM),Barcelona,Catalonia,Spain;Departmentof PsychiatryandForensicMedicine,UniversitatAutònomadeBarcelona,Barcelona,Catalonia,Spain

ODepartmentofPsychiatry,SchoolofMedicine,UniversityofOviedo-CentrodeInvestigaciónBiomédicaandReddeSaludMental,CIBERSAM,Oviedo,Spain

PSGDPBuilding,InstituteofPsychiatryPsychologyandNeuroscience,Kings'CollegeLondon,London,England

QDepartmentofPsychiatry,TrinityCollegeDublin,SchoolofMedicine,Dublin,RepublicofIreland

RDept.ofPsychiatry,UniversityofOviedo,SchoolofMedicine,Psychiatry,Oviedo,Spain

SThome,KlinikundPoliklinikfürPsychiatrieundPsychotherapie,UniversitatsmedizinRostock,Rostock,Germany

TStockholmCenterforEatingDisorderR&DUnit,DepartmentofClinicalNeuroscience,KarolinskaInstitutet,Stockholm,Sweden

UOsloUniversityHospital,DepartmentofRareDisorders,NevSom-NorwegianCentreofExpertiseforNeurodevelopmentalDisordersandHypersomnias, Oslo,Norway

VÖrebroUniverity,SchoolofMedicalSciences,CampusUSÖ,Örebro,Sweden

WNationalInstituteofMentalHealth,Klecany,CzechRepublic;ThirdFacultyofMedicine,CharlesUniversityPrague,CzechRepublic

XAntwerpUniversity(UA,CAPRI),Boechout,Belgium

YDepartmentofNeurologyandPsychiatry,SapienzaUniversityofRome,Rome;DepartmentNSMOS,FacultyofMedicineandPsychology,University

“Sapienza”ofRome,Rome,Italy

ZCenterforNeurodevelopmentalDisordersatKarolinskaInstitutet(KIND),CAPResearchCenter,Stockholm,Sweden

1JagiellonianUniversityMedicalCollege,SectionofAffectiveDisorders,DepartmentofPsychiatry,Krakow,Poland

2CambridgeAdultADHD&ASDClinic,Cambridge,England

3GehaMHC,Petach-Tikva,Israel

4UniversityCollegeDublin,Dublin,RepublicofIreland

5OutpatientClinic,Ottobrunn,Germany

6KlinikumKassel,DepartmentofPsychiatryandPsychotherapy,Kassel,Germany

7NovaMedicalSchool.UniversidadeNOVALisboa,Lisboa,Portugal

8NationalandKapodistrianUniversityofAthensMedicalSchool,EginitionHospital,DepartmentofPsychiatry,Athens,Greece

9INS,InstituteofNeuroscience,Florence,Italy

10HasanKalyoncuUniversity,PoyracıkSokak.Istanbul,Turkey

11LundUniversity,ClinicalSciencesLund,ChildandAdolescentPsychiatry,Lund,Sweden

12HighSecurityHospital,CRPLesMarronniers,Tournai,Belgium

ARTICLE INFO

Articlehistory:

Received9July2018

Receivedinrevisedform2November2018 Accepted3November2018

Availableonline16November2018

Keywords:

AdultADHD

UpdatedEuropeanConsensusStatement Diagnosis

Treatment

EuropeanNetworkAdultADHD EPA

ABSTRACT

BackgroundAttention-deficit/hyperactivitydisorder(ADHD)isamongthemostcommonpsychiatric disorders of childhood that often persists into adulthood and old age. Yet ADHD is currently underdiagnosedandundertreatedinmanyEuropeancountries,leadingtochronicityofsymptomsand impairment,duetolackof,orineffectivetreatment,andhighercostsofillness.

MethodsTheEuropeanNetworkAdultADHDandtheSectionfor NeurodevelopmentalDisorders AcrosstheLifespan(NDAL)oftheEuropeanPsychiatricAssociation(EPA),aimtoincreaseawarenessand knowledgeofadultADHDinandoutsideEurope.ThisUpdatedEuropeanConsensusStatementaimsto supportclinicianswithresearchevidenceandclinicalexperiencefrom63expertsofEuropeanandother countriesinwhichADHDinadultsisrecognizedandtreated.

ResultsBesidesreviewingthelatestresearchonprevalence,persistence,geneticsandneurobiologyof ADHD,threemajorquestionsareaddressed:(1)WhatistheclinicalpictureofADHDinadults?(2)How shouldADHDbeproperlydiagnosedinadults?(3)HowshouldadultADHDbeeffectivelytreated?

ConclusionsADHDoftenpresentsasalifelongimpairingcondition.ThestigmasurroundingADHD, mainly due to lack of knowledge, increases the suffering of patients. Education on the lifespan perspective,diagnosticassessment,andtreatmentofADHDmustincreaseforstudentsofgeneraland mentalhealth,andforpsychiatryprofessionals.InstrumentsforscreeninganddiagnosisofADHDin adultsareavailable,asareeffectiveevidence-basedtreatmentsforADHDanditsnegativeoutcomes.

Moreresearchisneededongenderdifferences,andinolderadultswithADHD.

©2018TheAuthor(s).PublishedbyElsevierMassonSAS.ThisisanopenaccessarticleundertheCCBY- NC-NDlicense(http://creativecommons.org/licenses/by-nc-nd/4.0/).

1.Introduction:theEuropeanNetworkAdultADHD

TheEuropeanNetworkAdult ADHD (ENAA) was foundedin 2003tohelp improvethediagnosisand treatmentofADHD in adultsinEuropeandbeyond.ENAArepresentsmentalhealthcare professionalsandresearchersfrom28countrieswithexpertiseon ADHD in adults (www.eunetworkadultadhd.com). The SectionNeurodevelopmentalDisordersAcrosstheLifespan(NDAL) oftheEuropeanPsychiatricAssociation(EPA)joinedoureffortto

provide this update of ourfirst Consensus Statement onadult ADHDpublishedin2010[1].

1.1.Objectivesoftheupdatedconsensusstatementforclinicians Despitestrongevidenceontheclinicalpresentation,genetics, neurobiology,theburdenofthedisorder,andonsafeandeffective treatment for ADHD in adults, many people are still under- diagnosedandundertreated.Specializedclinicalservicesremain scarceinmostpartsoftheworld,includingEurope[2,3].Ouraimis toprovideanupdateoftheliteratureonassessmentandtreatment ofadultADHDto[1]increaseawarenessonADHDasanimpairing life-longneurodevelopmentalconditionuptooldage[2];update

* Correspondingauthorat:EuropeanNetworkAdultADHD,VUMc,Amsterdam, EPA,TheNetherlands.

E-mailaddress:s.kooij@psyq.nl(J.J.S. Kooij).

(3)

theassessmentprocedurefordiagnosingADHDinadults;and[3]

giveupdatedrecommendationsforappropriatetreatments.

1.2.Methodology

Creatinga ConsensusStatementdoesnotfollowthe same procedureasrequiredforthedevelopmentofaguideline,such as systematic reviews using formal ratings of the evidence.

Mostoftheauthorsparticipatedinthedevelopmentofafirst ConsensusStatementonadultADHDin2010,andwereasked toprovideanupdateoftheprevioustextbasedonnewfindings in the literature since the time of publication. Subgroups dealing with differentsubjects were formed. The subgroups reached consensus on the text among themselves before sendingittothefirstauthor.Thefirstauthorputallparagraphs together and edited the text with the help of a few other coauthors(DW,SY,PA,DB).Thisdraftofthemanuscriptwas send to all authors for their comments. The first author checkedthecommentsandimplementedadjustmentsintothe text,andsendthefinalversiontoallauthorsforagreement.All authorsagreedwiththefinalversion.

2.Heritabilityandenvironment

Family,twinandadoptionstudiesfromthelast20yearsshow thatADHDisafamilialdisorderwithhighheritability,indicating that a significant genetic component influences risk for the disorder[4–12].Environmentalfactorssuchassevereinstitutional deprivationare alsolikely toplaya role, eitheras main causal factorsina few cases[13] orby interactionwithgeneticrisks.

Familystudiesindicatearisktofirst-degreerelativesof4–5fold thepopulationrateorhigher,withprevalenceratesaround20%

amongfirstdegreerelatives[14].DataonADHDinchildrenand adolescentsfindaverageheritabilityofaround76%[12].Studiesin adulttwinsusingself-ratedADHDsymptomsconsistentlyreport lowerestimatesofheritability,around30–40%[15–17].Onereason forlowerheritabilityofadultself-reportedADHDsymptomsmay befromtheuseofself-ratings.Theseleadtolowerestimatesof heritability compared to informant ratings regardless of age, perhapsdue to variablelevelsof awareness among individuals ratingtheirownADHDsymptoms[18,19].Studiescombiningdata acrossinformants [20], or using clinicaldiagnostic information [21]findheritabilityestimatesforadultADHDinthesamerange (70–80%)asforchildren[22].

2.1.Candidategenes

EarlymoleculargeneticstudiesofADHDinchildrenreported geneticassociationswithseveralcandidategenes.Geneticvariants withinorneartheD4andD5dopaminereceptorgenesprovided the most consistent findings supported by meta-analysis [23].

Otherspecificcandidategeneswereimplicatedintheearlystudies [12,24,25],butnonehaveprovidedconsistentevidenceorbeen replicated in more recent large-scalegenome wide association studies.Takentogether thetraditional neurotransmittersystem genesappear toexplainonlyasmallamountofthevariancein ADHD[26].Thereisalsosomeconvergingevidencefortheroleof genes that fit into a neurodevelopmental network involved in directedneuriteoutgrowth[27].

2.2.Genomewideassociationstudies(GWAS)

More recent findings have emerged from genome-wide associationstudies[28].Themostrecentdatasetreportedincluded over20,000ADHDcasesand35,000controls.Thesedatawereused to estimate that around 30% of the heritability of ADHD is

explained by common genetic variation. In total, twelve loci achieved genome-wide significance, including FOXP2; notable becausepriorworkhadimplicateditinadultADHD[29].These findings placeADHDfirmlyonthepathtodetectingverylarge numbersofassociatedcommongeneticvariantsasmoresamples areaccrued.

LD regression analyses that estimate genetic correlations betweendisorders findstronggeneticlinksbetweenADHDand arangeofoutcomesincludingeducationalperformance,depres- sion,obesity,smokingandlungcancer[28].Afurtherfindingisthe verystronggeneticcorrelationbetweenthediagnosisofADHD, andtraitscoresingeneralpopulationsamples,demonstratingthat ADHDrepresenttheextremeofacontinuouslydistributedtraitin thegeneralpopulation[30].Thesefindingconfirmthepolygenic natureofgeneticliabilitytoADHD.

Rarecopynumbervariants(CNVs)occurringonlessthan1%of chromosomesarealsoknowntoplayaroleinasubsetofindividuals withADHD[31,32].CNVswerefoundtobe2-foldmorecommonin children withADHDwithinthenormalIQrange,and6-foldhigherin thosewith IQsbelow70[32]. Specificgenes suggestedasCNVs linkedtoADHDincludethenicotinicalpha-7acetylcholinereceptor gene (e.g., [33]), several glutamate receptor genes [34] and neuropeptide-Y[35],althoughthesefindingsremaininconsistent andhardtoverifyduetolowfrequencyinthepopulation.

2.3.MoleculargeneticstudiesofadultADHD

MoleculargeneticstudiesofadultADHDarelessadvanced,but areexpectedtoconfirmsomegenetic associations identifiedin childhood and find othergeneticassociationsrelated topersis- tenceorremissionofADHDinadultlife[20].Apreliminaryreport attheInternationalNeuropsychologymeeting(Washington,2018) foundthegeneticcorrelationbetweenchildandadultADHDtobe greater than 80%. Most of the current research has been coordinatedin EuropebyBarbara Frankefrom theNetherlands fortheInternationalMulticentrePersistentADHD Collaboration (IMPACT) group.Thiscollaborationhassuccessfullygenerateda multi-sitesampleof morethan3500 patientsand continuesto grow.Todateseveralpublicationshighlightpotentialassociations withadultADHD,somebutnotallofwhicharesharedwithgenetic associationfindingsinchildren[36–42].

2.4.Environmentalfactors

Ithasbeenknownforalongtimethatenvironmentalfactors areassociatedwithADHD[43],particularlyprenatalriskfactors suchasexposuretoalcoholanddrugs,valproicacid,highblood pressure,maternalstressduringpregnancy,aswellaspreterm birth and low birth weight [44–46]. However sophisticated studydesignsareneededtoclarifywhethertheseassociation reflectdirecteffectsof the environmentalexposureor reflect genetically correlated risk measures. For example, although smokingduringpregnancyisclearlyassociatedwithoffspring ADHD,thisassociationappearstobeentirelyaccountedforby the genetic correlation between maternal smoking and off- spring ADHD [47]. In contrast, evidence from Romanian adoptees suggests that severe early deprivation is causally related to ADHD in a dose dependent way [13]. Gene by environmentinteractions(GxE)havebeenproposedandmay explain some of the missing heritability seen between heritabilityestimatesderivedfromtwin(0.76)andmolecular genetic(0.22)data.However,todatenoGxEeffectshavebeen clearlyidentified.Thefindingstodateindicatethatmuchmore work isneeded to understand the interplaybetween genetic andenvironmentalrisks.

(4)

3.NeurobiologyofADHD

3.1.Neuro-imaging:evidenceforatypicalgrayandwhitematterareas StructuralbrainscansofadultswithADHDshowedgreymatter abnormalitiesinseveralbrainareas,includingtherightfrontaland prefrontal areas [48,49], anterior cingulate [50–52], the basal ganglia and the cerebellum [53–56] with some preliminary research also showing abnormalities of the visual cortex [57].

Additionally,corticalthicknesswasfoundtobereducedinadult ADHD [56,58,59]. Some evidence suggests that grey matter abnormalities,insomesubcorticalregions,aremorepronounced in children than adults. This might reflect the effects of age, medication,intrinsicheterogeneityof theADHDsyndrome,ora combinationthereof[51,60–64].

Despite these reported findings the latest mega-analysis conducted by the Enigma consortium found no significant differencesinbrainstructurebetweenadultADHDandcontrols;

although,smallbutsignificantdifferenceswerefoundinchildren for subcortical regions including the accumbens, amygdala, caudate, hippocampus, putamen and intracranial volume with effectsrangingfromd=.10–.15[65].Thesefindingsindicatethat whiletherearestructuralchangesinsubcorticalbrainregionsin ADHDinchildren,thesearerelativelysubtleeffectsthatdissipate withincreasingage.

Diffusiontensorimaging(DTI)highlightedthatwhitematter tracts, including fronto-occipital, fronto-striatal, temporal and temporo-occipitalfasciculiandpartofthecorpuscallosum,bear microstructural abnormalities [66–71]. Additionally, some find- ingsalsolinkedmicrostructurevariabilitytosymptomatologysuch that greater inattention but not hyperactivity-impulsivity was associatedwithsignificantlylowerfractionalanisotropy(thatis lowermicrostructuralintegrity)intheleftuncinateandinferior fronto-occipitalfasciculicomparedtocontrols[70].Theseresults indicatethatstructuraldeficitsinADHDarenotjustconfinedto specificregions but involve interconnectionsamong largescale brainnetworks[68,71–73].

3.2.Functionalneuroimaging

Regarding functional MRI (fMRI) studies, task-based and resting-statefindings converge.Meta-analysesshowthatADHD isassociatedwithdysfunctionsinseveraldomain-specificfronto- striatal and fronto-cerebellar neural networks. Thus a meta- analysisof39childand16adultADHDfMRIstudiesconcludedthat inADHDtherearesignificantdysfunctionsinmultipleneuronal systemsinvolvedin higher-levelcognitivefunctions[74].These include hypoactivations in the frontoparietal executive control network, putamen, and ventral attention network, which is consistent with the classical model of ADHD as a disorder of deficientfronto-striatalactivation.

Hyperactivationsarealsoseeninregionsofthedefaultmode andvisualnetworks,whichsupportthecontemporaryviewthat ADHDisassociatedwithfaultyregulationofrelationshipsbetween defaultmodeand taskpositivenetworks.Similarfindingscome from meta-analyses, which show consistent underactivation in inferior fronto-striatalnetworks during cognitive tasks [75], in dorsolateral fronto-striato-parietal networks during attention tasks[75],andinfronto-cerebellarnetworksfortimingfunctions [76]; in addition to abnormallyenhanced activation in default moderegions[76].

The recent focus on resting state fMRI (RS-fMRI) identified multipleintrinsicneuralcircuits,reflectingfunctionalconnectivity withinandbetweenregionswhichiscontinuouslyencodedinthe spontaneousactivityofthebrain[77].Theintrinsicfronto-parietal, dorsalattentional,visual,motorand default modenetworksall

overlapwithregionsshowingdifferentialtaskactivationsduring inhibition,attention,orworkingmemorytasksinADHDcompared tocontrols[78].Despitethewealthofestablishedfindingsfrom fMRIandRS-fMRIstudiesofADHD,cross-sectionalneuroimaging dataiscorrelationalinnatureandcausalinferencescannotyetbe made.

More recently outcome studies of children diagnosed with ADHDhasbeenabletocomparefunctionalbrainchangeinadults withpersistent andremittedADHD and comparethesetoage- matchedcontrols.Thelargestsuchfollow-upstudytodate,of205 children with ADHD, found that persistence of ADHD was associated with loss of the balance of connections within the defaultmodenetwork,andconnectionsbetweenthedefaultmode andthosesupportingattentionandcognitivecontrol.Incontrast therewerenodifferencesinthesenetworksbetweenthosewhose ADHDhadremittedandnon-ADHDcontrols[79].

Overall,despitethewealthofestablishedfindingsfromfMRIand RS-fMRI studies of ADHD, cross-sectional neuroimaging data is correlationalinnatureandcausalinferencescannotyetbemade. The finding that certain functional brain changes areseen to differ betweenpersistentcomparedtoremittedcasesofchildhoodADHD shedssomelightonlikelycausalprocesses,butfurtherlongitudinal dataisstillrequiredbeforefirmconclusionscanbedrawn.

3.3.Neuropsychologicalandelectrophysiologicaltests

Asagroup,individualswithADHDarecharacterizedbyaltered neuropsychological functioning across a variety of executive function (EF) measures. However, thus far there is neither a neurobiologicalnoraneuropsychologicaltest(battery)forADHD withsufficientpositivepredictivepowertoestablishthediagnosis at the individual level [80]. In one study, the vast majority of neuropsychological instruments showed poor discriminative ability compared to clinical assessment measures such as the ASRS Screener v1.1 and the DIVA 2.0 Diagnostic Interview for ADHD in adults, withanoverall classification accuracyranging from53%to66% [81].Nevertheless,when usedincombination withtheDIVA2.0,objectivecognitiveperformancetestsmeasur- ingomissionandcommissionerrors,andphysicalactivity,were foundtoincrease thecorrectclassification ofadultADHD [81].

There is currently insufficient evidence to warrant the use of neuropsychologicaltesting todeterminethediagnosisof ADHD [82]ortopredictimpairmentinmajorlifedomains[83].

Moreover,cliniciansshouldalsobeawareofthepossibilitythat a few individuals may feign ADHD symptoms togain external incentives,likestimulantmedicationorspecialacademicaccom- modations.Thereissomeevidencesupportingtheeffectivenessof performance validity tests (PVTs) in differentiating between genuineandfeignedADHDcomparedtoratingscales[84].

Electrophysiologicalstudiessuggestthatbraindysfunctionsare involvedinthecentralcomponentsofADHDinbothchildrenand adults [85–89], although the finding of increased DAT density remainscontroversial[90,91].

DatafromElectroEncephalography(EEG)isrelativelyscarcein adultADHD.Generally,EEGstudiesofADHDfindsimilardeficitsin adults and children, while somefindings change withage and mightbesensitivetodevelopmentalchanges[92].DespiteUSFood and DrugAdministrationapprovalofanEEGdevice(2013)that assistsinthediagnosisofADHDsubtypes[93–95],this remains controversial[96].EEGtestsarenotsufficientlyaccuratebutcould beusefultoincreasediagnosticcertainty.

4.ICDandDSMcriteriaforADHD

TherearetwodiagnosticmanualsusedtodiagnoseADHD:The DiagnosticandStatisticalManualofMentalDisorders(DSM)and

(5)

theInternationalStatisticalClassificationofDiseasesandRelated HealthProblems(ICD).AsADHDhasbeenrecognizedasadisorder affectingindividualsacrossthelifespan,thediagnosticcriteriafor adolescents and adults have been adjusted in the DSM-5, publishedinMay2013:

1)ADHDis now inthechapter NeurodevelopmentalDisorders, whichincludesconditionsassociatedwithfactorsaffectingthe braindevelopment.

2)Diagnosticcriteriahavebeenadaptedbyaddingsomeexamples describing how ADHD symptoms are expressed across the lifespan.

3)Theageofonset criteriahasbeenchangedrequiringseveral symptomstobepresentbeforeageof12years,insteadofsome symptomsandimpairmentbyage7.

4)The term “subtype” has been replaced by “presentation”, reflectingthevariation ofADHD symptomswithinthesame individualduringthelifespan.

5)The symptom threshold required has been reduced to 5 symptoms instead of six for older adolescents and adults (>17years)ineithertheinattentionorhyperactive/impulsive domain.

6)Criteriarequiringsignificantimpairmenthasbeenmodifiedto

“clearevidence that symptoms interferewith or reducethe qualityofsocial,academicandoccupationalfunctioning”,with specifiersregardingseveritylevel.

7)ThepresenceofAutismSpectrumDisorder(ASD)isnolongeran exclusion criterion, consistent with evidence showing their frequentco-occurrence.

8)ADHDNotOtherwiseSpecified(NOS)hasbeenchangedinto OtherSpecifiedADHDandUnspecifiedADHD.

TherevisionofICD-10,ICD-11hasbeenpublishedinJune2018.

ICD-11,developedbytheWorldHealthOrganizationnowrefersto ADHD as Attention Deficit Hyperactivity Disorder, instead of previouslyHyperkineticDisorder(HKD)[97].Itnowusessimilar requirementsastheDSM-5regardingageofonset,andthesame3 presentation types. In Europe, ICD codes are often used for statisticsonmortality, morbidityandby insuranceagenciesfor health-relatedreimbursements [98], whereas DSM is primarily usedin clinicalpracticeby licensedmental health careprofes- sionals[99].

Thediagnosticassessmentstartsbyevaluationofself-reported symptomatology.Theclinicalinterviewisessentialfordiagnosing ADHDinadults,whichinvestigatesthecharacteristicsymptoms andimpairmentsofADHDin bothchildhood andadulthood.In childrenandadolescents,informants’ratingsarehighercorrelated withheritabilityandcognitiveandEEGfindingsthanself-ratings [19].Alsoprevalenceandpersistenceratesincreasewhenparent reportsareused[19].Inadultsthismaybeslightlydifferent,as someresearchshowsthattheadultpatientisthebestinformant [100].Thepresenceofafamilymemberhowever(aparentand/or the partner) during the assessment can still provide valuable additional information, e.g. on severityand its translation into dailyactivities.

There is compelling evidence that a cut-off of four current symptomsisthemostappropriateforanadultdiagnosis[101,102].

However, due to concern about the possibility of an artificial increase in theprevalence of the disorder, DSM-5 loweredthe thresholdfordiagnosingADHDfromsixtofivesymptomsforthose olderthan17yearsofage.Severalitemshavebeenexpandedby some illustrative examples to facilitate the recognition of the disorder throughout development. Although not included in thecriteria as such, behaviors reflecting executive dysfunction usually appear clearly during the assessment, when patients describeproblemswithorganization,facingdailyresponsibilities,

solvingproblems,managingtimeandself-regulating(inhibiting) behaviors.

DSM-5 also highlights the importance of mood lability and emotionaldysregulationas“anassociatedfeaturethatsupportthe diagnosis”.Althoughemotionaldysregulationmaydominatethe clinicalpresentation[103–105],itisnotacriterionforclassifying individualsasitlacksspecificity,occurringinmanyothermental healthconditions.

DSM-IV required that symptoms and impairment were presentbeforeage7,butasresearchdemonstratednodifferences betweenchildrenwithanageofonsetbeforeandafterage7[106]

thiscriterionwaschangedtoseveralsymptomsbyage12.Similar findingshavealsobeenreportedregardingadultsreportinglater- onset of symptoms [107,108],and there is disagreement both within and acrosssourcesconcerning recallof symptomonset [109].The fact that adultswithADHD frequently fail torecall childhoodbehaviorledtothesuggestionthatclinicianstakenote that the onset of the disorder was during the developmental period,ortheyshould useage16yearsastheupperagelimit.

UsingthiscriteriacapturedallcasesofchildhoodADHDand99%

ofadultswiththedisorder[110].ThedecisionofDSM-5toextend theageofonsetto12insteadof16mayhaveanegativeimpacton adultswithADHDwhohavedifficultieswithretrospectiverecall ofchildhoodbehaviors,andmaynotreceivethediagnosisforthis reason. This maybeparticularly true for thosewho hadsome compensation due to high intelligence, or lived in a highly structured or supported environment, or presented predomi- nantlywithinattentivesymptoms.Insuchcases,thepresenceofa collateral informant (generallya parent or spouse) is of great value. Many adults with ADHDthat are used to their lifelong symptoms, have limited awareness of how ADHD symptoms adverselyimpacttheirinterpersonalrelationshipsandaffecttheir life;somereportinghighersymptomsbutlowerimpairmentsor viceversa.

Suchinconsistencyhasbeenattributedtoalackofintrospec- tionandanincoherentself-view[111,112],andsupportstheutility of a collateral informant. If a significantother is not available, schoolreportsorsocialcarereportsmaybehelpful.

4.1.Clinicalpicture

4.1.1.Inattentionandhyperfocus

Patientswithmainlyinattentionproblemsare oftenslowto thinkandformulateduetodistractions.Theymayformulatethings in a long-winded and tangential way, losing themselves in irrelevant details and having difficulty making decisions. A difficultyfortheclinicianisthatthismayhinderthediagnostic assessment. Patients mayalsoover-concentrate or ‘hyperfocus’. This phenomenon most commonly occurs when engaged in activitiesthat thepatient finds very interestingand/or provide instantgratification,suchascomputergamesoronlinechatting.

Forsuchactivities,concentrationmaylastforhoursonend,ina veryfocusedmanner.

4.1.2.Hyperactivity

Withrespecttohyperactivity,adultsdonotpresentinthesame wayaschildren.Theirhyperactivityusuallymanifestsinamore subtleway.Cliniciansneedtoassesstheirfeelingsofrestlessness.A firstimpressionofmobilityisnotdefinitive;sittingcalmlyduring thediagnosticassessmentdoesnotexcludeanyADHD.Hyperac- tivityinadultsoftenmanifestsitselfasfeelingsofcontinuousinner restlessness or agitation, talking too much, ceaseless mental activity, notbeing abletorelax properlyor needingalcohol or drugstorelaxand/orsleep.Hyperactivityand/orrestlessnessmay betemporarilyrelievedbythepatientengaginginexcessivesport activities, and in such cases the person may suffer physical

(6)

ailmentsasthebodymayhaveinsufficienttimetorecoverand/or duetosustainedinjuries.

4.1.3.Impulsivity

Impulsivebehaviorandassociatedinterpersonalconflictsoften haveconsequencesforrelationshipswithfamily,friends,colleagues andemployers.Itmayalsoseriouslyimpactonpersonalfinance whenimpulsivespendingcausesdebt.Impulsivebingebehaviors mayalsobepresent(e.g.bingeeating),oftentocombatrestlessness ordue to a needfor immediate gratification. Closely relatedto impulsivityare‘sensationseeking’behaviorswhenpatientsmay seekoutexcitementfromnovelandthrillingstimuli.Theseoften involverisk takingbehaviors such asplaying with fire, reckless driving,sexualrisks,andprovocativebehaviorleadingtofights.

4.1.4.Emotionaldysregulation

EmotionaldysregulationislistedbyDSM-5asacharacteristic feature of ADHD, supporting the diagnosis [113]. The type of emotionaldysregulationseeninADHDhasbeencharacterizedas deficientself-regulationofemotionalsymptomssuchasirritabili- ty, frustration and anger [114], and low frustration tolerance, temperoutbursts,emotionalimpulsivity,andmoodlability[115].

Emotional dysregulation in ADHD is different from episodic symptomssuchasmarkedsustainedirritabilityoccurringwithin the context of altered mood states, such as an episode of depression or mania. In ADHD, emotional symptoms tend to reflectshortlivedexaggeratedchanges,ofteninresponsetodaily events, withrapidreturn tobaselinewithin a fewhours [114].

Whether the type of emotional instability seen in ADHD is qualitativelydifferenttothatseeninotherchronicconditionssuch asborderlinepersonalitydisorderorpost-traumaticstressremains unclear.

4.1.5.Excessivemindwandering

Another common feature of adult ADHD is excessive mind wandering,alsoreferred toasmentalrestlessness [116–118]. In DSM-5mindwanderingisbrieflymentionedastheoccurrenceof unrelated thoughts. Although mind wandering is a universal experience, some forms of mind wandering are detrimental becausetheyinterferewithtaskperformance.AdultswithADHD frequently report a distractible mental state with multiple unrelatedthoughtsthatareconstantlyonthegoandjumpfrom onetopictoanother[119,120].Mindwanderingisalsoafeatureof other mental health disorders such as depressive or obsessive disorders.However,inADHDmindwanderingischaracterizedby unfocused, shortlived distractible thoughts with nopattern of repeatedthoughtsorabnormalityofcontent.Researchfoundthat excessive mind wandering was strongly correlated with ADHD symptoms,wasastrongpredictorofthediagnosis(sensitivityand specificityaround90%forcase-controldifferences),co-variedwith ADHD symptoms over a 6-month period, and was a better predictorofADHD-relatedimpairmentsthantheinattentiveand hyperactive-impulsivesymptomsofADHD[120].InADHDitcan be measured using the Mind Excessively Wandering Scale [116,118,120](Table1).

4.1.6.Behavioralself-regulation(executivefunctiondeficits) ADHDhasbeendescribedasadisorderofexecutivefunctions suchasinhibitionandworkingmemory.Theseincludeproblems organizing,prioritizingand initiatingwork;focusing,sustaining and shifting attentionto tasks;regulating alertness,sustaining effortandprocessingspeed;managingfrustrationandregulating emotions; utilizing working memoryand accessing recall; and monitoring and self-regulation of behavior [121,122]. Although clinicallythesearegooddescriptionsof thetypesof difficulties experiencedby adultswith ADHD,behavioral measuresdo not

correlate well with cognitive or neuropsychological tests of executive control [121–123]. A distinction needs to be made between rating scale measures of behaviours reflecting self- regulationofbehaviorreferredtoasEF(behavioral)deficits,and theresultsofneurocognitivetestsofEFssuchasworkingmemory andinhibition.Neuropsychologicaltestscoresreflectingexecutive functioninglackecologicalvalidityinthattheyhavenosignificant relationshiptobehaviouralratingscalemeasuresofEF[124].The EF testscoresalsoare verypooratpredictingimpairment ina variety of domains of major life activities, compared to EF behaviouralratingscales[125].

4.1.7.BurdenofADHD

TheimpairmentsassociatedwithADHDacrossthelifespanare impressive.ADHDisassociatedwithlearningdifficulties,school dropout,underachievementatwork[126],frequentjobchanges [127], chronic fatigue [128],financial problems, gambling and Table1

ExamplesofADHD-relatedsymptoms.

Inattention Forgetfulness Distractibility Chaoticpresentation

Difficultyorganizing&planning Difficultylistening

Difficultywithpunctuality(arrivingeithertoolateortoo early)

Temporaryhyperfocusforhighlysalienttasks,butno controlofattentionwhenrequiredorformanyessential activitiesofdailylife

Gettinglostindetails

Doubtfulnessunabletomakedecisionsorsolve problems

Needingtoomuchtimetocompletetasks Difficultystartingandfinishingtasks MindWandering:

Mentalrestlessness

Unrelatedspontaneousthoughts,constantlyonthego, jumpingandflitting,multiplethoughtsatthesame time

Associativethinking

Hyperactivity (Inner)Restlessness Difficultyrelaxing Pacingupanddown Talkingtoomuchandtooloud Fidgeting,rockingortapping

Notbeingabletobearanofficejobbecauseof restlessness

Knockingthingsoverbecauseofexcessivemobility Beingabletositstillbutthiscomeswithmusclestrain Restlesssleep

Impulsivity Actingwithoutthinking

Difficultywaitingturnlinkedtofeelingsofirritability Blurtingthingsoutthatcausedistresstoothers Interruptingothers

Impatienceanddifficultywaitingturn Spendingtoomuch

Walkingoutofjobs Startingrelationshipsquickly Notbeingabletopostponegratification Sensationseekingandrisktakingbehaviors Bingeeating

Emotional dysregulation

Moodlability

Lowfrustrationtolerance Emotionalimpulsivity Irritability

Angeroutbursts

Premenstrualincreaseofsymptoms

(7)

internet use [129,130], home and traffic accidents leading to increasedmortalityrates[131–133],relationshipdifficultiesand intimate partner violence [134,135], early onset of addiction [136], teenage pregnancies and sexual transmitted diseases [137,138],atwo-foldincreasedsmokingrate[139],anincreased number of suicide attempts and self-harm in adolescents [140,141],andincreasedcriminality[142,143].Moreover,physical disordersandailmentsmaybecomechronicduetoforgetfulness, healthproblemsinducedbyanegativelifestyle,pooreatingand sleeping habits, and lack of health care follow-up [144–147].

ADHDhasfurtherbeenassociated withauto-immunediseases [148],obesity[149], andphysical multi-morbidity.Inonelarge study,individualswithmorethan4diseaseshadovermorethan 3-foldhigheroddsofpossibleADHD[146].Theriskofdiabetes, hypertension,cardiovasculardiseaseandcancer,thatarerelated toobesity, maybe increased aswell. Anadditionalburdenon familylife maybe the presenceof one or more childrenwith ADHD,whichhappensfrequentlyduetothehighfamilialrisksof thedisorder.

Cliniciansshouldalsobeawarethathighfunctioningadultswith ADHDmaynotpresentwithatypicalpatternoffunctionalimpair- mentsintheirdailylife.Adaptiveorcompensatoryskillscandevelop thatmaskthemoreovertbehavioralproblemsrelatedtoADHD[150].

Somemayfindworkthatiswellsuitedtotheir symptomprofile.

Furthermore,inADHDneurocognitiveperformanceandinattentive symptomsaresensitiveto thesalienceoftaskactivities[151,152].Such people with ADHD mayexcel in certain aspects oftheir lives, but still be impairedinothers,suchasmoreroutineandmundanetaskssuchas paying bills, looking after the house, or developing stable social relationships.Problemscanincludesubjectivedistressfromsymp- tomssuchasmentalandphysicalrestlessness,sleepproblems,and emotionalinstability;andtheuseofdrugssuchascannabisoralcohol toreducethesesymptoms.

5.PrevalenceofADHDacrossthelifespan

In childhood, ADHDis among themostcommonpsychiatric disorderswithaprevalencerateof3–5%[153].Forthisagegroup, wellestablisheddiagnosticandtreatmentservicesareavailable throughoutmostofEurope.Inthelastfourdecades,alargebodyof evidencehasaccumulated,showinghowinthemajorityofcases ADHDis a lifespandisorder, persistingaseither thefullblown disorder, or in ‘partial remission’ with persistence of some symptomsandcontinuedclinicalandpsychosocialimpairments [154–161]. The prevalence of ADHD in adults across twenty countrieswasrecentlyestimatedat2.8%,witharangebetween1.4 -3.6%[3].ADHDwasalsofoundinaDutchpopulationstudyto persistinto oldage(>60years) withaprevalence of 2.8–4.2%

dependingoncut-off(6or4currentsymptomsrespectively),and associatedwithimpairment[162–166]. ADHDin olderadults is accompaniedbyincreasedratesofmoodandanxietysymptoms, generalhealthproblems,conflicts,divorce,loneliness,andalower income,showingasimilarpatternofproblemsasinyoungerage groups.Researchexploringtheneedsfortreatmentofolderadults withADHDhascommenced,andthefirsttreatment protocolof olderadultswithADHDhasbeenpublished[167].

5.1.Sexissues

SexdifferencesinADHDdiagnosisarewelldocumented,withgirls beinglesslikelytobediagnosed,andsexratiosrangingbetween1:5to 1:9[168].Suchdiscrepancyislessevidentinepidemiologicalresearch inchildrenwherethesexratiois1:3,suggestingunderrecognitionof ADHDingirlsintheclinic.Inbothepidemiologicalandclinicalstudies ofadultADHDthesexratioiscloserto1:1[169].Severalfactorsmay explainthesexdisparityduringthelifespan.GirlswithADHDmay

have lesshyperactive/impulsive symptoms than boys;because of higherdisruptiveness,boysaremorelikelytobereferredbyparents and teachers, whereas girls remain undiagnosed [170]. Missed diagnosismay bedueto a lackof knowledgeandrecognition of ADHDingirlsbyhealthcareprofessionals,andto thepresenceofother conditions:lowself-esteem,anxietyaswellaffectivedisordersoccur frequently in females with ADHD, and it is possible that ADHD symptoms may be mistakenly attributed to such comorbidities [171,172]. Females with ADHD appear to develop better coping strategiesthanmales,andarebetterabletomasksymptomsofADHD throughoutchildhood.However,thismaynolongerworkwellwhen theyfacesalientlife challenges,suchasleavingschool, attending collegeoruniversity,commencingemployment,managingintimate relationships,andtakingresponsibilityfortheirownlifedecisions [173]. Different genetic liability betweenthe sexes [174], as well neuroendocrinefactorsaffectingthedopaminergicsystem,suchas thyroidandestrogenhormones [172,175],haveallbeenalsosuggested toplayaroleinthemaskingofADHDingirlsandwomen.Inaddition, girlsandwomenwithADHDarelesswellstudiedthanmales.

Women with ADHD are particularly vulnerable to early adversities, health and mental health problems compared to controls [176]. A higher prevalence of insomnia, chronic pain, suicidalideation,generalizedanxietydisorder,depressivedisor- ders,agreatervulnerabilitytonicotinedependence[176,177]and anincreasedlikelihoodofriskysexual behaviors[138]hasbeen reportedinwomenwithADHDincomparisonwithcontrols.

5.2.Transitionofadolescentstoadultmentalhealthservices Astwo-thirdsormoreofchildrenwithADHDcontinuetohave impairmentintoadulthood[178],manyrequirethetransitionfrom childtoadultmentalhealthservices.However,transitionbetween servicesisgenerallydifficult,placingyouthswithADHDinaneven morevulnerableposition[179].Researchshowsthatdisruptionof careduringtransitionadverselyaffectsclinicaloutcome[180,181].

Clearrecommendationshavebeenformulated,mostlybasedon clinicalexperience, tofacilitatesuccessfultransition ofpatients withADHDfromchildtoadultmentalhealthservices[1,182–185].

Thesearea)transitionshouldideallybecompletedbytheageof18 years,b)transitionshouldbeplannedinadvancebybothchildand adultmentalhealthservices,c)youngpeoplewithADHDandtheir parentsshouldhavesufficientinformationregardingthetransition process (e.g. psychoeducational material including available services), d) both continued parental care and child’s growing autonomyshouldbeconsidered,e)ifnecessaryaformalmeeting involving child and adultmental health services (with specific knowledgeonthisagegroup)andpatientsandparentsshouldbe considered.Allthesecanhelptopreventthedrop-outofyoung peoplewith ADHD fromservices. However,the realityis quite different,asindicatedbytworeviews[186,187].Comparedtoother diagnosticgroups,youthwithADHDweresignificantlylesslikely to be referred, they were more likely to refuse referral, and a significantnumberremainedinchildserviceswellbeyondtheir 18th year. Studies also have found transition policy deficits [186,188],suboptimalexperienceoftransitionwhenitdoesoccur [186,189], adearthof adultADHD services[190],and a lackof expertiseonADHDamongstadultclinicians[3,191].Thissuggests there isanurgent needfora multifacetedapproach combining transitionspecificclinicalguidelines,andfundingforthetraining thetrainingofclinicians,toensurethatthoseinneedofongoing interventionmaysuccessfullytransitiontoadultservices.

5.3.Late-onsetADHD?

Recent longitudinalstudies haveindicatedthat besidestypical childhoodonsetADHD,withthefulldiagnosticcriteriabeingmet

(8)

beforetheageof12years,theremaybelater-onsetcaseswithonsetof the full diagnostic criteria beyond this age [104,189,190]. These findings have provencontroversial due to severemethodological limitations[192,193],howeverthelargemajorityoflateronsetcases appeartomeettheDSM-5ageofonsetcriteriaofseveralsymptomsby theageof12[113].Lateonsetofsymptomswasevaluatedinthe controlarmofthelong-termfollow-upoftheMultimodalTreatment studyofADHD(MTA).Inmostcases,otherfactorswerepresentthat coulddiscountthelateonsetofADHDsymptomsandexcludethe diagnosis of ADHD [194], such as symptoms representing non- impairingcognitivefluctuations,acomorbiddisorder,orthecognitive effectsofsubstanceuse[192].However,thereremainedaverysmall sampleofadolescentonsetcases.Anotherpopulationcohortstudy foundthatthemajorityofthosewithapparentlate-onsetADHDhad highADHDscoresatleastonepointinchildhood,suggestingthatthey mayhavebeenmisclassifiedonthebasisoftheirscoreatage12years [195].Thesecaseswithhighscorebeforetheageof12yearsmightnot havemetfullcriteriabeforetheageof12years,butwouldmeetthe current DSM-5 criteria for several symptoms in childhood. One conclusion is that clinicians should be aware that subthreshold cases of ADHD during childhood might go on to meet the fulldiagnostic criteria as older adolescents. Clinicians should take care to fully assess impairment,psychiatrichistory,andsubstanceusewhendiagnosing andtreatingcaseswithapparentlater-onsetADHD[192].

6.Screeninganddiagnosticassessment

6.1.Screening

Severalscreeningtoolsareavailable forADHDinadults.The validatedtoolrecognizedbytheWorldHealthOrganization(WHO) and updated for DSM-5 criteria is the Adult ADHD Self report RatingScale(ASRS).Thisrevised ASRSwas studiedin managed care,thegeneralpopulationandinaclinicalgroup.Thesensitivity was 91.4%; specificity 96.0%; AUC, 0.94; PPV, 67.3% [196]. The previous version of the ASRS has been translated into many languages (see http://www.hcp.med.harvard.edu/ncs/asrs.php).

TheWenderUtahRatingScaleassessesbesidesADHDabroader spectrum of symptoms that often accompany ADHD or are comorbid. Several other scales that ask about the 18 items as definedintheDSM-5toclassifyADHDareavailable,seeTable2.

AkeyquestioniswhoshouldbescreenedforADHD.Ingeneral, sincethehallmarkofadultADHDisachronictrait-likecondition that emerges out of childhood or early adolescence, anyone presentingwithsuchaclinicalpictureshouldbescreened[2].This shouldincludethosewithchronichistoriesofinattentive,restless orimpulsivebehaviors,aswellasthosewithemotionalinstability.

TargetedgroupswhereratesofADHDaresignificantlyincreased and should therefore be screened include family members of people with ADHD, and those with a history of behavioral problems,anychronicmentalhealthdisorderincludinganxiety,

depression, cyclothymia, personality disorder, bipolar disorder, substance use disorders, those with multiple physical diseases [146],andthosewithinthecriminaljusticesystem[197].

6.2.Diagnosticassessment

For diagnostic assessment, the use of a semi-structured diagnosticinterviewisadvised,suchastheDiagnosticInterview forADHDinadults,secondedition(DIVA2.0)[198],basedonthe DSM-IV-TR criteria.DIVA2.0is availableonlinewithoutcharge, currentlyin19languages(www.divacenter.eu).TheConner’sAdult ADHD Diagnostic Interview for DSM-IV (CAADID) has been validatedinEnglishandSpanish[199].DIVA2.0hasbeenvalidated intwoEuropeanpopulations[81,199],andisincreasinglyusedin internationalresearch.ADIVA2.0appisavailableintheAppand GooglePlaystores.TheupdateofDIVA2.0forDSM-5criteriainto

‘DIVA-5’inalllanguagesisongoing.DIVA-5-ID,for peoplewith Intellectual Disability (ID) and Young DIVA, for children and adolescents,arenewversionsofDIVA-5. Analternativeis ACE+

(http://www.psychology-services.uk.com/resources.htm),asemi- structured diagnostic interview toassess ADHD in adults (>16 years). ACE+assesses the core symptoms of ADHD in both adulthood and childhood, the extent to which they impair functioning,and thepresenceofco-existing conditions.ACE+is currentlyonlineavailablein7languages,withmoretranslations underway.Fortheseandotherdiagnostictools,seeTable2.

6.3.TheassessmentprocessofADHDandcomorbidity

Diagnosisof ADHDisbasedonacarefulandsystematicassessment ofalifetimehistoryofsymptomsandimpairment.Centraltothis process is the assessment of childhood-onset and current symptoms of ADHD,andthepresenceofsymptomsandimpairmentinatleasttwo domains (school, work, home, interpersonal contacts). For this lifetime assessment,collateralinformationfromfamilymembersandspouse areuseful.Itisimportanttotakeafullmedicalhistoryofpsychiatric andsomaticconditions,aswellasafamilyhistoryofpsychiatricand neurologicalproblems.Highintelligenceshouldbetakenintoaccount asapotentialmoderatorinthediagnosticassessment,asADHDis underdiagnosedinpatientswithhighintelligencebecausetheyuse morecompensatorystrategies[200].Cliniciansshouldalsobeaware thathighfunctioningadultswithADHD may not present witha typical pattern of functionalimpairments intheir dailylife. Adaptive or compensatoryskillscandevelopthatmaskthemoreovertbehavioral problemsrelatedtoADHD[150].Somemayfindworkthatiswell suited to their symptom profile. Furthermore, in ADHD neurocognitive performanceandinattentivesymptomsaresensitivetothesalienceof taskactivities[151,152].SuchpeoplewithADHDmayexcelincertain aspectsoftheirlives,butstillbeimpairedinothers,suchasmore routine andmundanetaskssuchaspayingbills,lookingafterthe house,ordevelopingstablesocialrelationships.Problemscaninclude

Table2

OpenaccessScalesandInterviewsforDiagnosticAssessmentofADHDinadulthood.

Scalesa

AdultADHDSelf-ReportScale DevelopedbyWHO;6-itemversion,basedon DSM-5(ASRS),inmanylanguages

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470397/

WenderUtahRatingScale https://www.thecalculator.co/health/Wender-Utah-ADHD-Rating-Scale-Calculator-858.html DiagnosticInterviewsb

DIVA-5 StructuredDiagnosticInterviewforADHDinadults;accordingtoDSM-5;in19languageswww.divacenter.eu ACE+ Semi-structuredInterviewforADHDinadultshttps://www.psychology-services.uk.com/adhd.htm

aOtherscaleswithoutopenaccessare:ConnersAdultADHDRatingScale(CAARS),andtheAdultADHDInvestigatorRatingScale(AISRS).

b Otherinterviewswithoutopenaccessare:ConnersAdultADHDDiagnosticInterview(CAADID),AdultADHDClinicalDiagnosticScale(ACDS).

Hivatkozások

KAPCSOLÓDÓ DOKUMENTUMOK

[1] Mason, M., Walker, L., Wine, L., et al.: Child and adolescent to- bacco and substance use within the context of ADHD: implica- tions for prevention and treatment. A., Barkley,

Introduction: European guidelines on the treatment of Neisseria gonorrhoeae are based mostly on Western European data, although these recommendations may not be optimised for

Here we have shown that chronic treatment with an MVT preparation improved well established diagnostic markers of diabetes such as fasting blood glucose, HbA1c, glucose tolerance,

Diagnosis of U-HAE is purely based on clinical findings and requires that patients have the (i) above-mentioned clinical symptoms, (ii) one or more family members also affected

To our knowledge, this study is the first to investigate the level of dyskinesia by comparing a stimulant-treated and a treatment-naive ADHD group of children. Our

In this paper, we try to answer the following questions: (1) to what extent do treatment seeking SUD patients with adult ADHD, compared to those without adult ADHD, have a delayed

1.) I am the first one, who analyzed the effects of QoL and subthreshold disorders in case of children who were referred for psychiatric evaluation but did not fulfill

Psychiatric comorbidity in treatment seeking substance use disorder patients with and without ADHD: results of the IASP study.. * the first two authors contributed equally to