ADHD: Oversigt over de seneste 20 års research

Denne artikel er baseret på Cortese et al., (2018) og er en opdatering af forskningen om ADHD i de sidste to årtier, idet der tages hensyn til alt relateret til forståelse, diagnosticering og behandling af ADHD. En skal læses for alle, der har lyst til at kende en ting eller to om, hvad ADHD virkelig er, gør og forårsager.

Kilde: Cortese, S., & Coghill, D. (2018). Twenty years of research on attention-deficit/hyperactivity disorder (ADHD): looking back, looking forward. Evidence Based Mental Health21(4), 173–176. https://doi.org/10.1136/ebmental-2018-300050

BEMÆRK: Denne artikel er auto-oversat via Google Translate, så hvis noget virker lidt kludret formuleret, så er dette grunden til det, ikke min manglende evne til at formulere mig 😉

ABSTRAKT

I denne kliniske gennemgang opsummerer vi, hvad der efter vores mening har været nogle af de vigtigste fremskridt inden for de sidste to årtier med hensyn til diagnostisk definition, epidemiologi, genetik og miljømæssige årsager, neuroimaging / cognition og behandling af ADHD, herunder:

(1) De seneste ændringer til de diagnostiske kriterier i Diagnostisk og Statistisk Manual for Mental Disorders og International Classification of Diseases;

(2) Meta-analytiske beviser, der viser, at ADHD-frekvenserne er ret konsekvente i de vestlige lande efter regning af diagnostiske metoder.

(3) Den seneste undersøgelse af det første GWAS fandt betydelige risk-loci for ADHD;

(4) Paradigmeskiftet i den patofysiologiske konceptualisering af ADHD fra ændringer i individuelle hjerneområder til en kompleks dysfunktion i hjernenetværk;

(5) Beviser, der understøtter den kortvarige effekt af ADHD farmakologiske behandlinger, med en anden profil af effekt og tolerabilitet hos børn / unge mod voksne;

(6) En række meta-analyser, der viser, at selvom ikke-farmakologisk behandling muligvis ikke er effektiv til at målrette ADHD-kerne symptomer, adresserer nogle af dem effektivt ADHD-relaterede svækkelser (såsom modstandsdygtige adfærd for forældreuddannelse og arbejdshukommelsesunderskud for kognitive uddannelse).

Vi diskuterer også nøgleprioriteter for fremtidig forskning inden for hvert af disse undersøgelsesområder.

Alt i alt skal mange andre spørgsmål besvares, mens mange forskningsspørgsmål er blevet besvaret.

Styrkelse af tværfaglige samarbejder, der er baseret på store datasæt i åben videnskabs ånd og støtte forskning i ugunstigt stillede lande, vil være afgørende for at imødegå de udfordringer, der står i vejen.

INTRODUKTION

Attention deficit/hyperactivity disorder (ADHD) er den mest almindelige neurodevelopmental lidelse hos børn, med en estimeret verdensomspændende prævalens omkring 5%.

Selv om det i lang tid er blevet betragtet som en barndomsforstyrrelse, er det nu fastslået, at forringelse af ADHD-symptomer vedvarer i en stor del af tilfælde (ca. 65%), selv om der er variabilitet i estimatet på grund af metodisk heterogenitet på tværs af undersøgelser.

Hvad angår andre psykiske lidelser har der i de sidste to årtier været en stigende undersøgelse af ADHD. Årsagerne til denne stigning er: øget anerkendelse af ADHD’s virkning på funktionen; fremskridt inden for forskningsmetodik og teknologi; og interesse fra farmaceutiske virksomheder.

Her giver vi et overblik over, hvad vi anser for at være nogle af de vigtigste fremskridt i de sidste to årtier i ADHD-forskning. Vi diskuterer også nøgleområder for fremtidig forskning.

METODER

Given the large body of literature and space constraints, this review is selective rather than systematic and comprehensive. We relied mostly on meta-analyses, retrieved with a search in PubMed using the following syntax/terms (update: 8 August 2018): (ADHD OR Attention Deficit OR Hyperkinetic Disorder) AND (meta-analy* OR metaanaly*).

DIAGNOSTISK DEFINITION

Den diagnostiske og statistiske manual for psykiske lidelser, femte udgave (DSM-5), offentliggjort i 2013, introducerede flere væsentlige ændringer i forhold til DSM fjerde udgave tekstrevision (DSM-IV-TR) 5 kriterierne.

For det første blev tærsklen i antallet af symptomer (kriterium A), der var nødvendige for diagnosen hos ældre unge og voksne, reduceret fra 6 til 5.

Denne ændring er i tråd med den opfattelse, at på trods af en reduktion af antallet af symptomer over udvikling kan voksne med ADHD i barndommen stadig frembyde forringelse.

Den krævede alder for begyndelsen blev øget fra ‘forud for 7’ til ‘før 12’.

Formålet med disse ændringer var velegnet og designet til at lette diagnosticeringsprocessen hos voksne, som ofte har problemer med at bestemme den nøjagtige alder for starten, især hvis de er tidlige i udviklingen.

Desværre var hverken forandring baseret på empiriske beviser, og metoder til diagnostisk opgørelse hos voksne er stadig under debat.

En anden pivotal ændring i DSM-5 er fjernelsen af ​​vetoet om den dobbelte diagnose af ADHD- og autismespektrumforstyrrelser (ASD), der var til stede i tidligere udgaver af DSM.

I modsætning til alder af udbrud og ændring af symptomnummer ændres denne ændring af en betydelig undersøgelse.

Endelig blev de (sub) typer af ADHD, der er defineret i DSM-IV- (TR), erstattet af forestillingen om forskellige præsentationer.

Dette anerkender ustabiliteten i den fænotypiske manifestation af uopmærksomhed eller hyperaktive / impulsive symptomer over tid i modsætning til den mere statiske opfattelse af en subtype.

Med hensyn til den internationale klassificering af sygdomme (ICD) ser det ud til, at vetoet til diagnosticering af ASD i tilstedeværelsen af ​​ADHD vil blive bevaret i den kommende ICD 11. Revision.

Alt i alt, mens disse ændringer til en vis grad afspejler de seneste empiriske beviser og / eller praktiske behov i diagnostikprocessen, er der stadig problemer, der skal løses.

For det første fokuserer de nuværende kriterier stadig på antallet af symptomer frem for en mere præcis definition af funktionssvigt. Dette bør være en prioritet for området og indsatsen, såsom udviklingen af ​​den internationale klassifikation af funktion, handicap og sundhed: Børne- og ungdomsversion, er allerede igangværende.

For det andet, mens i øjeblikket hver af de symptomer, der er anført i DSM-kriterium A, bærer samme vægt, er det blevet hævdet, at uopmærksomheden burde være mere vægtet end hyperaktivitet / impulsivitet. Støttende beviser, der kommer fra kliniske prøver, skal replikeres i befolkningsbaserede undersøgelser.

For det tredje er det uklart, hvordan man bedst kan integrere forskellige informationskilder (f.eks. Forældre, lærere osv.). At løse denne udfordring er afgørende.

For det fjerde, selv om det foreslås som en separat type ADHD eller endda en separat diagnostisk enhed, er det stadig uklart, hvorvidt konstruktionen af ​​træg kognitivt tempo (nedsat opmærksomhed hos hypoaktive udseende personer) overlapper ADHD uopmærksom præsentation.

Endelig er et af de mest kontroversielle emner på hele området for ADHD-forskning i øjeblikket omkring muligheden for, at ADHD kan opstå de novo i voksenalderen, i modsætning til dets konceptualisering som en neuro-udviklingsforstyrrelse.

Trods et stigende antal vigtige studier er kontroversen langt fra at blive løst, og vi regner med, at det vil være et stort fokus for forskning på området i de kommende år.

Vi forventer også, at de foreslåede radikale, selvom kontroversielle ændringer i den nosografiske tilgang til mentale sundhedsmæssige forhold, såsom forskningsdomæne kriterierne, vil påvirke den fremtidige forskning om ADHD væsentligt.

EPIDEMIOLOGI

Et af de mest kontroversielle spørgsmål i forbindelse med epidemiologi af ADHD har eksisteret om mulige forskelle i forekomsten af ​​lidelsen i forskellige lande.

I særdeleshed citeres differentieringsraten for klinisk diagnose i Nordamerika og Europa af adhærere af ADHD, som understøtter forestillingen om, at ADHD ikke er en “ægte” lidelse, men snarere en social konstruktion.

En meta-analyse, der blev offentliggjort i 2007, viste dog, at diagnostiske kriterier, informationskilde, krav til nedsættelse for diagnoser og geografisk oprindelse af undersøgelserne var signifikant påvirket af den estimerede poolede ADHD-værdi (5,29%).

En signifikant forskel i forekomsten opstod kun mellem Nordamerika og både Afrika og Mellemøsten, selv om bevis fra ikke-vestlige lande var begrænset.

Da der imidlertid kun var et begrænset antal undersøgelser til rådighed for Afrika og Mellemøsten, bør disse resultater tages i betragtning med forsigtighed.

Derimod opstod der ingen signifikante forskelle mellem Europa og Nordamerika, hvilket tyder på, at når der anvendes den samme diagnostiske tilgang, er sygdomsraten forholdsvis konsistente i de vestlige lande, hvor variabiliteten i forekomsten primært skyldes metoder til diagnosticering af ADHD.

En anden nyere meta-analyse fandt ingen beviser til støtte for en stigning i den epidemiologiske forekomst af ADHD i de sidste tre årtier, når standardiserede diagnostiske procedurer følges.

Dette indebærer, at tendensen for øgede diagnosetrin ikke regnes med reelle stigninger i prævalensen.

Derimod er misforholdet mellem de administrative og epidemiologiske sygdomsproblemer, der varierer mellem USA og Europa, sandsynligvis tegnet af kulturelle og sociale faktorer.

Da størstedelen af ​​de tilgængelige epidemiologiske undersøgelser fokuserer på børn i skolealder fra Nordamerika og Europa, bør der opfordres til yderligere befolkningsbaserede studier fra andre kontinenter såvel som i førskolebørn og voksne.

Derudover vil langsigtede epidemiologiske undersøgelser, der tager sigte på en bedre forståelse af udviklingssporerne og forudsigelserne for remission / persistens af ADHD i voksenalderen, være instrumental sammen med andre kliniske, neuropsykologiske, genetiske og neuroimaging-undersøgelser for at informere forebyggelsesprogrammer.

Udvikling af en standardiseret definition af caseness og remission vil være afgørende for, at denne forskningsgruppe er frugtbar.

GENETISKE ÅRSAGER AF ADHD

Studier af tvillinger og adopterede børn indikerer en høj arvelighed for ADHD (60% -90%).

Bestræbelser på at finde de gener, der understøtter denne arvelighed, har været mere udfordrende end oprindeligt forventet.

Hvad angår andre mentale sundhedsmæssige forhold, blev det klart, at ADHD ætiologi står for et komplekst samspil mellem mange gener hver med en relativt lille effekt og ved gen × miljøinteraktioner.

Den første tilgang til at finde generne involveret i ADHD var ‘kandidatgen’-tilgangen. Denne fremgangsmåde fokuserer på at identificere varianterne i gener kodende for proteiner hypotese, der tidligere er involveret i patofysiologien af ​​ADHD. Disse undersøgelser identificerede kun omkring 10 gener som en betydelig støtte, som sammen tegnede sig for kun en lille del af den samlede ADHD-arvelighed.

Den næste store tilgang, “genomsamlede associeringsundersøgelser” (GWAS), som gør det muligt at analysere et stort antal almindelige (dvs. til stede hos mere end 5% frekvens i befolkningen) enkeltnukleotidpolymorfier over hele genomet, var i første omgang mislykket i ADHD, da den tilgængelige prøve var for lille til at vise en meningsfuld virkning.

I et stort gennembrud er de første 12 uafhængige loci for nylig blevet identificeret gennem GWAS.

Foreninger blev beriget i intolerante intolerante gener og hjerneklarede regulatoriske mærker, der banede vejen for en række nye undersøgelseslinier om ADHD’s neurobiologi.

En yderligere nyligt udviklet tilgang fokuserer på sjældne (dvs. en frekvens i befolkningen under 1%) ‘copy number variants’ (CNV). Disse defineres som replikationer eller deletioner af DNA’et med en længde på mindst 1 kb. CNV’er, der er overrepræsenteret i ADHD, er blevet påvist, men deres bidrag kan hidtil kun forklare 0,2% af ADHD-arvelighed.

MILJØMÆSSIGE ÅRSAGER TIL ADHD

Hvad angår miljømæssige etiologiske faktorer har der i de seneste år været betydelige data, der tyder på, at prænatale og postnatalfaktorer, såsom rygning til mødre og alkohol, lav fødselsvægt, for tidlig fødsel og eksponering for miljømæssige toksiner, såsom organophosphatpesticider, polychlorerede biphenyler og zink, er forbundet med øget risiko for ADHD.

Med undtagelse af for tidlig fødsel har genetiske undersøgelser imidlertid impliceret uimodede familielle konfronterende faktorer, som ikke er i overensstemmelse med en årsagssammenhæng i miljøfaktorer.

Alvorlig modermangel har også været relateret til udviklingen af ​​ADHD-lignende symptomer.

Undersøgelsen af ​​årsagerne til ADHD har stadig mange ubesvarede spørgsmål. Vi har brug for en bedre forståelse af, hvordan gener interagerer med hinanden og om samspillet mellem miljøfaktorer og gener.

Genetik har potentialet til at tilbyde mange andre spændende fremtidige forskningsveje i ADHD.

Vi nævner kun kort her:

(1) anvendelsen af ​​induceret pluripotent stamcelle afledt fra perifert væv hos patienter med ADHD og bruges til at generere hjerneceller med det formål at model hjerne kredsløb og reaktioner på medicin eller andre stressorer;

(2) brugen af ​​zebrafisk og frugtflue-modeller for at udvide de nuværende dyremodeller af ADHD.

NEUROIMAGING

Første patofysiologiske modeller af ADHD, der blev offentliggjort for 20 år siden, var baseret på dysfunktioner i et begrænset antal hjerneområder, nemlig frontal cortex og basale ganglier.

I løbet af de sidste to årtier og lignende andre psykiske sygdomme er et stort paradigmeskift fra ændringer i de enkelte hjerneområder til dysfunktion i hjernenet blevet begyndt at omforme vores forståelse af patofysiologien af ​​ADHD.

Strukturelt viste meta-analyser og mega-analyser af de strukturelle MR-undersøgelser, der blev udført i løbet af de sidste to årtier, at konsekvent replikerede ændringer i basalganglierne og i en række andre subkortikale områder.

Funktionelt viste en omfattende meta-analyse, at størstedelen af ​​de ADHD-relaterede hypoaktiverede områder var relateret til ventral opmærksomhed og frontoparietale netværk.

I modsætning hertil faldt flertallet af ADHD-relaterede hyperaktiverede områder inden for standardmodusnetværket, og andre hyperaktiverede områder var inden for det visuelle netværk.

Dette er i tråd med den hypotese, at opmærksomheden bortfalder, der karakteriserer ADHD, skyldes et uhensigtsmæssigt indtrængen af ​​standardnetværket i aktiviteten af ​​opgaver-positive netværk, frontoparietale, ventrale eller dorsale opmærksomhedsnetværk, ifølge standardnetværkshypotesen af ​​ADHD, som har været uden tvivl et af de mest inspirerende forslag i neurovidenskaben i ADHD i løbet af de sidste to årtier.

Mens vi har fået indsigt i hjernenetværkene, der er dysfunktionelle i ADHD og i forsinkelsen i kortikal modning, ser vi frem til den næste generation af neuroimaging-undersøgelser, som vi håber, vil begynde at oversætte disse resultater til den kliniske praksis.

Indførelsen af ​​maskinindlæringsmetoder, som f.eks. Støttevektormaskine, er blevet hilst velkommen inden for klinisk neurovidenskab som en måde at oversætte neurovidenskabelige fund på det enkelte patientniveau til og dermed overvinde hovedbegrænsningen af ​​aktuelle undersøgelser, der kun kan give resultater, der er gyldige på gruppen, snarere end individuel, niveau.

Et stigende antal undersøgelser har brugt maskinindlæring baseret på MR data for at validere diagnosen ADHD med varierende grad af succes.

NEUROCOGNITION

Neurokognitive undersøgelser har ydet et betydeligt bidrag til vores forståelse af ADHD.

I de seneste år har feltet flyttet væk fra lineære single-cause modeller af ADHD mod multipathway modeller, der fremhæver heterogeniteten iboende til ADHD og tilvejebringer en sammenhæng mellem individuelle forskelle på hjerneniveau og klinisk præsentation.

Vi mener, at en interessant forskningspolitik for fremtiden vil være at kombinere genetik, klinisk, neurokognitiv og neuroimaging data for at definere, via maskinindlæringsmetoder, respons på behandling, tolerabilitetsprofiler og funktionel bane af sygdommen over tid.

Dette vil være et afgørende skridt i retning af personlige og præcise tilgange til behandling.

BEHANDLING

Farmakologiske

I løbet af de sidste to årtier har der været en markant stigning i antallet af randomiserede kontrollerede forsøg (RCT) med henblik på at teste den kortsigtede effekt og tolerabilitet af farmakologiske behandlinger for ADHD (både stimulerende og ikke-stimulerende medicin).

De fleste er sponsoreret af Big Pharma og blev designet til at understøtte licensen til medicinen.

Parallelt på grund af bekymringer omkring mulige bivirkninger af medicin og manglende klarhed omkring deres langsigtede virkninger, er der udviklet flere forskningslinjer vedrørende ikke-farmakologiske interventioner.

Nylige vigtige metodologisk lydmeta-analyser giver os mulighed for at sammenfatte og kritisk diskutere denne store beviser.

For de farmakologiske interventioner viste en omfattende netværksmeta-analyse af 133 dobbeltblindede RCT’er høje til moderate effektstørrelser (hvad angår effektivitet) for de forskellige lægemidler versus placebo.

Standardiserede gennemsnitlige forskelle (SMD) varierede fra -1,02 (95% CI -1,19 til -0,85) for amfetaminer til -0,56 (95% CI -0,66 til -0,45) for atomoxetin (methylphenidat: -0,78, 95% CI -0,93 til – 0,62).

Hos børn / unge var methylphenidat det eneste lægemiddel med bedre acceptabilitet end placebo; hos voksne var det kun tilfældet for amfetamin (uden forskel mellem placebo og andre aktive lægemidler).

Under hensyntagen til både effektivitet og sikkerhed understøttede beviser fra denne meta-analyse methylphenidat som foretrukket første valg medicin til kortvarig behandling af ADHD hos børn / unge og amfetamin til voksne.

Ikke-farmakologiske

Hvad angår ikke-farmakologiske muligheder, er en omfattende syntese om ikke-farmakologiske behandlinger for børn og unge med ADHD blevet fremlagt i en række meta-analyser af den europæiske ADHD Guidelines Group (EAGG).

I 2013 offentliggjorde de en første systematisk gennemgang / meta-analyse, der behandlede effekten af ​​adfærdsmæssige interventioner, diætinterventioner (begrænsede eliminationsdietter, udelukkelse af kunstig madfarve og fri fedtsyretilskud), kognitiv træning og neurofeedback på ADHD-kerne symptomer (dvs. uopmærksomhed , hyperaktivitet og impulsivitet).

Den systematiske gennemgang omfattede kun RCT’er og betragtede to kontrasterende resultater: dem, der blev vurderet af personer, der ikke var blindet til behandlingsbetingelsen (aktiv vs kontrol) og dem, der var vurderet af personer, der sandsynligvis var blindet til behandling (fx lærere i forsøg, der vurderede en adfærdsmæssig intervention implementeret med forældre).

Resultaterne var påfaldende forskellige afhængigt af typen rater. Når man ikke overvejede blindede vurderinger, resulterede alle interventioner signifikant mere effektivt end kontrolbetingelsen med hensyn til reduktion af ADHD-kerne symptomer.

Men når man overvejer de mere strenge sandsynligvis blinde vurderinger, var kun fri fedtsyretilskud og kunstig farvefjernelse udelukkende væsentlig mere effektiv end kontrolbetingelserne med små effektstørrelser (henholdsvis SMD = 0,16 og 0,42), hvilket tyder på, at den kliniske virkning af Disse behandlinger på ADHD-kerne symptomer er på gruppens niveau beskedne.

Efterfølgende EAGG-meta-analyser fokuserede på ADHD-kerne symptomer og på ADHD-relaterede problemer. En metaanalyse, der specifikt fokuserede på adfærdsmæssige indgreb viste, at selv om man overvejer sandsynligvis blinde ratings, var adfærdsmæssige interventioner effektive til forbedring af vigtige aspekter i forbindelse med ADHD, nemlig forældremyndighed (SMD for positiv forældre 0.63, SMD for negativ forældre 0.43) og problemer (SMD 0,31).

En anden opdateret meta-analyse om kognitiv træning, som blev fundet effektiv til forbedring af verbal og visuel arbejdshukommelse, som er svækket i en stor del af børn med ADHD og er blevet påvist at adskille fra ADHD symptomer.

Disse meta-analyser tyder også på, at uddannelse, der retter sig mod flere neuropsykologiske aspekter, kan være mere effektiv til at forbedre ADHD-symptomer end at træne målrettet kun på et aspekt af kognitiv funktion.

Den seneste meta-analyse af EAGG på neurofeedback gav ikke støtte til effekten af ​​neurofeedback på nogen af ​​de neuropsykologiske og akademiske resultater.

Samlet set giver denne forskningsform ikke tilstrækkelig dokumentation til rutinemæssigt at anbefale ikke-farmakologiske interventioner som yderst effektive behandlinger for ADHD-kerne symptomer, selvom nogle af dem (f.eks. Adfærdsmæssige interventioner eller kognitiv træning) kan være effektive for vigtige tilknyttede svækkelser (oppositionsmæssige adfærd henholdsvis hhv. hukommelsesunderskud).

Fedtsyre-tilskuddets rolle og udelukkelse af kunstig madfarve som mulige behandlingsstrategier bør overvejes forsigtigt i betragtning af den lille effektstørrelse, med CI tæt på ikke-signifikans.

Det mest sandsynlige område for fremtidig behandlingsforskning i ADHD vil sandsynligvis være at få indblik i de langsigtede positive og negative virkninger af behandlinger ved hjælp af randomiserede forsøg med tilbagetrukne designs samt yderligere populationbaserede undersøgelser med selvstyrede metoder og longitudinelle opfølgende undersøgelser.

Disse skal klarlægge konklusionerne fra de forskellige opfølgende bølger i multimodal behandling af ADHD (MTA) undersøgelse, hvilket viser, at hverken typen og intensiteten af ​​behandlingen modtaget i den første 15-måneders randomiserede fase af undersøgelsen (behandling som sædvanlig medicinering ( MED), adfærdsterapi (BEH), medicin plus adfærdsterapi (COMB)) eller udsættelse for medicin over de efterfølgende observationsperioder forudsagde det funktionelle resultat ved opfølgning, der nu er udvidet til 16 år.

Af hensyn til MTA blev behandlingerne modtaget i de tre forsøgsarme (MED, BEH, COMB) i den første 15-måneders randomiserede fase omhyggeligt udformet med henblik på at opnå optimale resultater.

Efter denne indledende fase var alle deltagere frit at vælge den type behandling, de modtog fra deres faste udbyder.

Da det er sandsynligt, at disse behandlinger ikke blev så omhyggeligt optimeret og overvåget som de tre eksperimentelle grupper i den randomiserede fase, er disse længerevarende fund af MTA ikke letfortolkelige og kan til en vis grad være vildledende.

KONKLUSION

Mange spørgsmål er blevet besvaret korrekt inden for ADHD. Mange andre bliver stadig behandlet. Yderligere tværfaglige samarbejder, brug af store datasæt i Open Science’ ånd og støtte til forsknings-aktiviteter i mindre fordelagtige lande er nøglen til at løse udfordringen.

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Kollndorfer, K., Krajnik, J., Woitek, R., Freiherr, J., Prayer, D., & Schöpf, V. (2013). Altered likelihood of brain activation in attention and working memory networks in patients with multiple sclerosis: an ALE meta-analysis. Neuroscience and Biobehavioral Reviews, 37(10 Pt 2), 2699–2708. https://doi.org/10.1016/j.neubiorev.2013.09.005

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