Nasjonalt Kompetansesenter for AD/HD, Tourettes Syndrom og Narkolepsi - MULIGHET FOR MESTRING
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Nasjonalt Kompetansesenter for AD/HD,
Tourettes Syndrom og Narkolepsi
MULIG
HET FO
R MES
TRING
Grand Hotell, Oslo
15 års jubileumskonferanse
12 - 13 februar 2009
www.nasjkomp.noPROGRAM DAG 1 PROGRAM DAG 2
Torsdag 12. februar 2009 Fredag 13. februar 2009
Hele dagen foregår i Rococo-salen
10:00 - 10:20 Åpning av konferansen Parallellsesjoner
10:20 - 11:05 Long term Outcomes and Comorbidity. Lessons from the Parallell 1 ADHD og Tourettes syndrom (Rococo-salen):
MTA-study, Peter Jensen, MD, PhD - s. 14 08:30 - 09:15 Læringsstrategier og tilpasset opplæring, Vigdis Refshal,
11:05 - 11:50 Differentiating ADHD and Bipolar Disorder, cand.paed. - s. 39
Peter Jensen, MD, PhD - s. 21 09:15 - 10:00 IKT som hjelpemiddel, Bjørgulv Høigaard, cand.paed
11:50 - 12:00 Pause/ Benstrekk og Hedda Ekstrøm, cand.paed. - s. 41
12:00 - 12:45 Tourette Syndrome: From one phenotype to many, 10:30 - 11:15 Tiltak i skolen for barn med utfordrende atferd, - hvilke
Andrea Cavanna, MD, PhD - s. 29 muligheter har vi og hva vet vi? Morten Hendis, cand.polit - s. 43
12:45 - 13:30 Health-related quality of life in Tourette syndrome, 11:15 - 12:00 Tourettes syndrom og AD/HD - arbeid? Muligheter og
Andrea Cavanna, MD, PhD - s. 31 begrensninger, Hanne Gulbrandsen og Børre Hansen,
13:30 - 14:30 Lunsj psykologspesialister - s. 45
14:30 - 16:00 Narcolepsy and Hypocretin: Neurobiology, genetics and Parallell 2 Narkolepsi (Hambro):
immunology, Emmanuel Mignot, MD, PhD - s. 33 08:30 - 09:15 Forekomst av narkolepsi i Norge, Mona Skard Heier, dr.med. - s. 47
16:00 - 16:30 Pause 09:15 - 10:00 Narkolepsi hos barn, Mona Skard Heier, dr.med. - s. 49
16:30 - 17:30 Opplæring og evidensbaserte atferdstiltak - en oversikt, 10:30 - 11:15 Livskvalitet hos mennesker med narkolepsi i Norge,
Terje Ogden, professor - s. 35 Solveig Ervik, dr. scient. - s. 51
(Postersession utgår) 11:15 - 12:00 IKT som hjelpemiddel, Bjørgulv Høigaard, cand.paed og
Hedda Ekstrøm, cand.paed - s. 53
12:00 - 12:15 Pause
12:15 – 13:00 Plenum (Rococo-salen):
Panel Fellestrekk, utfordringer og ulikheter mellom AD/HD,
Tourettes syndrom og narkolepsi, Dr. Mignot, dr. Cavanna
og dr. Jensen. Ordstyrer: Geir Øgrim - s. 55
13:00 - 13:15 Avslutning
13:15: Lunsj
2 NK 3 NKVELKOMMEN ARRANGEMENTSKOMITE
Kjære konferansedeltakere!
Nasjonalt Kompetansesenter for AD/HD, Tourettes Syndrom og Narkolepsi ønsker dere hjertelig
Gerd Strand
velkommen til 15 års jubileumskonferanse. NK ble opprettet i 1994 som et resultat av godt Gerd Strand, leder av Nasjonalt Kompetansesenter for AD/HD, Tourettes Syndrom
samarbeid mellom Sosial- og Helsedepartementets Handlingsplan for funksjonshemmede og og Narkolepsi siden opprettelsen i 1994. Utdannet cand. polit. fra Universitet
Utdannings- og forskningsdepartementets omorganisering av de statlige spesialskolene. i Oslo, med bakgrunn som allmennlærer og spesialpedagog. Strand var en av
Det var tydelig at våre diagnoser hadde et stort behov for bedre utredning og behandling, og at initiativtakerne ved opprettelsen av ADHD Norge i 1979. Hun sitter i fagrådene
det var ganske tilfeldig hva slags hjelp som ble tilbudt rundt omkring i landet. Dette ville de to til både ADHD Norge og i Norsk Tourette Forening, og regnes som den som
departementer rette på. Egentlig skulle NK være et 3-årig prosjekt, men de tre årene har altså har jobbet lengst i Norge med Tourettes syndrom. Hun har redigert boka “AD/
blitt til 15. Vi startet i 1994 med 4 ½ stilling. Nå i 2009 er vi 6 faste og en stipendiat i full stilling. HD, Tourettes syndrom og narkolepsi – en grunnbok”. Gerd Strand er medlem
I tillegg har vi tre deltidsansatte. av “Nordisk ekspertgruppe for AD/HD” som ble opprettet i 1990 og “European
Society for the Study of Tourette Syndrome (ESSTS)” som ble opprettet i 2000.
En av våre viktigste oppgaver er informasjonsformidling gjennom kursvirksomhet, brosjyrer
og tidsskriftet ”Innsikt”, som kommer fire ganger i året. Til 10-års jubileet utga vi en bok som
heter ”AD/HD, Tourettes syndrom og narkolepsi – en grunnbok”. Denne boka har vi oppdatert Knut Hallvard Bronder
til dette jubileet. Vi har kalt konferansen ”Mulighet for mestring”. Vi ønsker alle å mestre livet
vårt – i familie, barnehage, skole, arbeid og fritid. For oss i NK er en av grunnpilarene at vi Utdannet sykepleier med videreutdanning i psykiatri. Arbeidet ved Blakstad
skal hjelpe mennesker med våre diagnoser til å mestre de forskjellige utfordringer livet gir og Dikemark sykehus. Hovedsakelig med langtidspasienter og administrasjon,
på forskjellige stadier og områder. Til å gi oss det siste innen forskning på AD/HD, Tourettes og som lærer ved sykepleierskole. Bronder har vært aktiv som tillitsvalgt
syndrom og narkolepsi, har vi fått forelesere som er blant de beste i verden: i pasientorganisasjonen ADHD Norge siden 1989, og var assisterende
Peter Jensen, MD, PhD, fra New York skal snakke om AD/HD. generalsekretær 2001-2009. Knut har arbeidet mye med AD/HD hos voksne, og i
Andrea Eugenio Cavanna, MD, kommer fra Birmingham for å snakke om Tourettes syndrom. forhold til politiske myndigheter, helsevesen, fengselsvesen og utdanningssektor.
Emmanuel Mignot, MD, PhD, fra Stanford University i USA foreleser om narkolepsi. Bronder var den første leder av AD/HD Global Network. Han er i dag rådgiver
Terje Ogden ved Universitetet i Oslo gir oss en oversikt over tiltak som har vist seg å virke ved på NK.
atferdsforstyrrelser hos barn og ungdom.
Å få en korrekt diagnose er viktig, men det har liten verdi hvis det ikke følges opp med gode
tiltak. Programmet dag to har flere foredrag om tiltak og hjelpemidler, men også om to studier Janne B Drage
på narkolepsi som er utført i regi av NK. Stipendiat/forsker på prosjektet om Tourettes syndrom og livskvalitet ved NK.
Konferansen avrundes med en paneldebatt der Peter Jensen, Andrea Cavanna og Emmanuel Drage er utdannet cand.polit., hovedfag i psykologi ved NTNU i Trondheim.
Mignot diskuterer fellestrekk, utfordringer og ulikheter ved våre diagnoser. Hun har tidligere jobbet med habilitering, rehabilitering, rus, kognitiv svikt og
dobbeltdiagnoser i Oslo kommune.
På vegne av arrangementskomiteen for jubileumskonferansen,
Bjørgulv Høigaard
Cand.paed. (1989) fra Universitet i Oslo og spesialist i pedagogisk-psykologisk
Gerd Strand rådgivning. Han har erfaring fra videregående opplæring, PPT, Utdanningsdirektorat
leder og departement. Bjørgulv Høigaard har vært tilknyttet Statped siden 1994 og
de siste årene har han arbeidet mye med opplæringstiltak for ungdom med
nevrobiologiske vansker. Han har deltidsstilling på Bredtvet kompetansesenter og
NK. Skribent i fagtidsskrifter og bøker, de siste årene spesielt om bruk av IKT som
lære- og hjelpemiddel.
4 NK 5 NKARRANGEMENTSKOMITE
NOTATER
Egil Midtlyng
psykologisk rådgiver på NK siden 2004. Utdannet cand. psychol. fra UiO, og
spesialist i arbeids- og organisasjonspsykologi. Foruten å ha jobbet med
rehabilitering og nevropsykologi, har han vært ansatt ved Statistisk sentralbyrå
med ansvar for rekruttering og opplæring av intervjuere og som prosjektleder for
ulike undersøkelser.
Hege Skoghus
kontorleder ved NK siden høsten 2008. Jobbet i grafisk bedrift i perioden
1997-2002 og tok deretter helsesekretærutdannelse. Var kontorleder ved
Nyremedisinsk avdeling fra høsten 2002 og har bred erfaring med arbeid ved
sengepost, poliklinikk, hemo- og peritonealdialyse.
Ståle Tvete Vollan
Kommunikasjonsrådgiver på NK og redaktør for INNSIKT. Vollan er cand.
philol. i musikkvitenskap fra NTNU i Trondheim i 1999 og har studert i litteratur,
historie og pedagogikk. Engasjement og erfaring for tilrettelegging har han
fra jobben som rådgiver for studenter med funksjonshemning ved NTNU i
2000/2001, hvor han bl.a. skrev en rapport om tilrettelegging av eksamen for
studenter. Vollan har arbeidet som foreleser og sensor ved NTNU, og som
vikarlærer på alle skoletrinn.
Ebba Wannag
EBBA WANNAG, overlege på NK siden 2002. Hun er cand.med. fra Universitetet
i Oslo (UiO) i 1967, og spesialist i barnesykdommer fra 1977. Ebba har årelang
erfaring med nevrologisk betingede sykdommer hos barn. Hun har særlig
interessert seg for sammenhengen mellom epilepsi og AD/HD hos barn og
unge.
Geir Øgrim
er nevropsykolog, konsulent for NK og til daglig enhetsleder ved Nevroteamet
BUP Østfold. Teamet betjener BUPPer i Østfold i form av veiledning, kurs
og spesialundersøkelser av barn og unge med nevropsykiatriske tilstander.
Øgrim er leder i det nasjonale fagrådet i ADHD Norge. Øgrim har skrevet flere
fagbokkapitler, bla. i 1. og 2. utgave av NKs fagbok, og artikler om AD/HD.
Øgrim arbeider med forskning på kvantitativt EEG og EEG biofeedback.
6 NK 7 NKFOREDRAGSHOLDERE FOREDRAGSHOLDERE
Peter S. Jensen, MD Emmanuel Mignot, MD, PhD
President and CEO, REACH Institute (Resource for Advancing Children’s Health) Professor of Psychiatry and Behavioral Sciences
New York, New York Howard Hughes Medical Institute Investigator
Director, Center for Narcolepsy
Peter S. Jensen, MD, is President, CEO, and founder of the REACH Institute (the Resource
for Advancing Children’s Health), From 1999 until mid-2007, Dr. Jensen was the Ruane Pro- Emmanuel Mignot is Professor of Psychiatry and Behavioral Sciences, Howard Hughes Medi-
fessor in Child Psychiatry at the Columbia University in New York, where he also served cal Institute Investigator and Director of the Center for Narcolepsy at Stanford University. Dr.
as the founding director of the Center for the Advancement of Children’s Mental Health. Mignot is on the editorial board of several journals and is active in multiple governmental and
Prior to coming to New York, Dr. Jensen was Associate Director, National Institute of Mental non-governmental organizations. He has served on NIH study sections, on the as Chair of the
Health (NIMH), for child and adolescent research, where he served from 1989 to 2000. At NIH National Sleep Disorder Center Advisory board, as President of the Sleep Research Soci-
NIMH he was the lead NIMH investigator on the Multimodal Treatment of ADHD study (MTA) ety and as a board member of the National Sleep Foundation. He currently chairs the Board
and an investigator for other NIMH multi-site national studies. He is currently a scientific of Scientific Councilors of the National Institute of Mental Health. Dr. Mignot has experience
advisor for CHADD (Children, Adolescents, and Adults with ADHD), NAMI (National Alliance in clinical and basic research in sleep disorders medicine.
for the Mentally Ill).
Dr. Mignot’s research led to the identification of HLA-DQB1*0602 as the main HLA susceptibil-
Dr. Jensen received his MD degree in 1978 from the George Washington University Medical ity factor in human narcolepsy. He is also known for pharmacologically dissecting the mode of
School in Washington, DC, and completed his post-graduate psychiatry and child psychiatry action of currently prescribed narcolepsy treatments such as antidepressants, amphetamine-
training in 1983 at the University of California, San Francisco. like stimulants, modafinil, and gammahydroxybutyric acid. Using a narcoleptic dog model,
his group was also the first to positionally clone a disease gene in dogs. The narcolepsy
Dr. Jensen serves or has served as a member of the Editorial Board of many journals in- gene was found to be a G-protein coupled receptor for the neuropeptides hypocretin/orexin, a
cluding Development and Psychopathology, Psychiatric Services, the Journal of the Ameri- system previously believed to be primarily involved in feeding regulation. Dr. Mignot‘s labora-
can Academy of Child & Adolescent Psychiatry, Journal of Child Psychiatry and Psychology, tory later demonstrated that human narcolepsy is associated with a deficiency in hypocretin
Journal of Child and Adolescent Psychopharmacology, Journal of Abnormal Child Psychol- neurotransmission. Dr. Mignot has received numerous awards for his work on narcolepsy and
ogy, and Biologic Psychiatry. Dr. Jensen’s main areas of interest include effectiveness and sleep disorders.
dissemination research, and assisting medical practitioners and parents to adopt evidence-
based mental health assessment and treatment approaches in dealing with children who
are suffering from mental disorders.
Terje Ogden, cand.paed, professor
Terje Ogden er forskningsdirektør ved Atferdssenteret, Unirand og professor II ved Psykolo-
Andrea Cavanna, MD, PhD gisk Institutt, Universitetet i Oslo.
Andrea Eugenio Cavanna, MD, is Consultant in Behavioural Neurology at the Department of Neuro-
psychiatry, Birmingham, and Honorary Research Fellow, University College London, United King-
dom. He currently is leading consultant for the Tourette clinic at the Department of Neuropsychiatry,
Birmingham. He has published extensively in the field of behavioural neurology and neuro-
psychiatry, with special focus on the behavioural aspects of Tourette syndrome and epilepsy. Vigdis Refsahl, cand.paed.
His other research areas include the neural correlates of altered conscious states in neuro-
psychiatric conditions. Jeg er utdannet cand.paed og arbeider som seniorrådgiver ved dysleksiteamet ved Bredtvet
kompetansesenter. Jeg har tidligere praksis fra PP-tjenesten. Jeg var 9 år i PPT og har nå
vært 8 år på Bredtvet. Jeg har siden jeg startet på Bredtvet kompetansesenter arbeidet med
tiltak for elever med dysleksi, men også med implementering av læringsstrategier skolen,
både i grunnskole og videregående skole, samt voksenopplæring. Forelesningen bygger mye
på de erfaringene jeg har gjort i dette arbeidet, særlig når det gjelder elever som strever på
ulikt vis, med motivasjon, skoleinnsats og faglig læring.
8 NK 9 NKFOREDRAGSHOLDERE FOREDRAGSHOLDERE
Hedda Ekstrøm, spesialpedagog Hanne Gulbrandsen, cand.psychol.
Hedda Ekstrøm har arbeidet ved lære-og hjelpemiddelteamet ved Bredtvet kompetansesent- Utdannet Cand.Psychol. ved Universitet i Oslo, 1987, spesialist i klinisk nevropsykologi
er siden 2003. Hun er særlig opptatt av hvordan bruk av datakompensatoriske hjelpemidler, Praksis fra Sunnaas sykehus HF Nesodden 1988 – 1997, Pedagogisk-psykologisk tjeneste,
som talesyntese og presentasjonsprogrammer, sammen med studietekniske strategier, kan i Oslo 6 måneder 1997 og NAV sitt Senter for yrkesrettet attføring, nevroteamet 1997 – d.d.
hjelpe elever med dysleksi eller språkvansker i skolearbeidet. Hun har direkte kontakt med Gulbrandsens spesialistoppgaver i NAV er: Arbeidssøkere med AD/HD og komorbid AD/HD
elever for utprøving og tilrettelegging av datamaskin og programvare. Hun holder kurs for og Tourettes syndrom: Nevropsykologiske forskjeller mellom gruppene, og nevropsykolo-
pedagoger i hvordan man intergrerer bruk av datakompensatoriske hjelpemidler i undervis- giske testersbetydning i vurdering av arbeidsevne.
ningen. Hun underviser også i Bredtvet kompetansesenters videreutdanning for lærere innen
digitale lære- og hjelpemidler i særskilt tilpasset opplæring. Hedda Ekstrøm er 51 år og av
utdanning har hun 2.avd spesialpedagogikk
Mona Skard Heier, dr.med.
Mona Skard Heier er spesialist i nevrologi og i klinisk nevrofysiologi. Hun har vært ansatt ved
Bjørgulv Høigaard, cand.paed. Ullevål sykehus i ca 25 år, de siste ca 15 årene som seksjonsoverlege ved klinisk nevrofysi-
ologisk laboratorium (KNF-lab). Ved KNF-laboratoriet ble det i 1994, under hennes ledelse,
opprettet et søvnlaboratorium hvor man særlig arbeidet med utredning og diagnostikk av
F. 1957 er cand. paed. (1989) fra Universitet i Oslo og spesialist i pedagogisk-psykologisk
søvnsykdommer knyttet til hjernens regulering av søvn.
rådgivning. Han har erfaring fra videregående opplæring, PPT, Utdanningsdirektorat og de-
Hun tok medisinsk doktorgrad i 1989, og har gjennom alle år som lege vært engasjert i for-
partement. Bjørgulv Høigaard har vært tilknyttet Statped siden 1994 og de siste årene har
skningsprosjekter. Som pensjonist har hun arbeidet med undervisning, foredragsvirksomhet
han arbeidet mye med opplæringstiltak for ungdom med nevrobiologiske vansker. Han har
og forskning innen søvnsykdommer, med hovedvekt på narkolepsi og beslektede hypersom-
deltidsstilling på Bredtvet kompetansesenter og NK. Skribent i fagtidsskrifter og bøker, de
nier. Hun har ca 70 publikasjoner innen søvnsykdommer og andre nevrologiske og nevro-
siste årene spesielt om bruk av IKT som lære- og hjelpemiddel.
fysiologiske emner, de fleste i internasjonale medisinske tidsskrifter. Sammen med dr. Anne
Wolland har hun skrevet boken ”Søvn og Søvnforstyrrelser” (Cappelen 2005 ).
Morten Hendis, cand.polit.
Morten Hendis’ fagområder er atferds- og lærevansker, samt minoritetsspråklige elever med
Solveig Ervik, dr. scient.
lærevansker. Han er også regionkoordinator for PALS i region øst. Solveig Ervik er utdannet dr. scient innen spesialpedagogikk og har arbeidet p Nasjonalt
Faglig fordyping: Sammenhengen mellom utredning og implementering av god praksis/en- kompetansesenter for ADHD, TS og Narkolepsi fra 1999 til 2007, de siste Ârene som forsker.
dringer på lærer, klasse og skolenivå. Barn og ungdom med utfordrende atferd, utredning og Hun er n leder av Nasjonalt kompetansesystem for d¯vblinde - Koordineringsenheten.
tiltak. Implementering av skoleomfattende endringer, veiledning og tiltaksutvikling
Utdanning: Spesialpedagog/Cand.Polit. 2-årig etterutdanning i nevropsykiatri.
Arbeidserfaring/Bakgrunn: Lærer i folkehøgskole, grunnskole og høgskolelektor i spesi-
alpedagogikk. Arbeidserfaring som konsulent både privat og i helse og sosialetat, som pros-
jektleder og prosjektmedarbeider og har siden 1993 vært PP-rådgiver i Valdres. Arbeidet som
rådgiver ved Øverby kompetansesenter i 1994 og avdelingsleder ved Torshov kompetanse-
senter fra 2000-2002. PP-rådgiver i Valdres igjen fra 2002-2006. Rådgiver ved Torshov kom-
petansesenter fra 2006. Regionkoordinator for PALS i region øst.
Børre Hansen, cand.psychol.
Børre Hansen er utdannet Cand.Psychol. fra Universitetet i Oslo i 2000 og er spesialist
i klinisk nevropsykologi. Han har vært ansatt ved Pedagogisk-psykologisk tjeneste i Oslo,
og arbeider nå i Nevroteamet ved NAV Senter for yrkesrettet attføring. Basert på en stud-
ie av klienter ved Nevroteamet skrev han sammen med kollega Hanne Guldbrandsen sin
spesialistoppgave ”Arbeidssøkere med AD/HD og komorbid AD/HD og Tourettes syndrom:
Nevropsykologiske forskjeller mellom gruppene, og nevropsykologiske testersbetydning i
vurdering av arbeidsevne.”
10 NK 11 NKDag 1
Torsdag 12 februar 2009
Rococo-salen, Grand hotel
“Mulighet for mestring”
12 NK 13 NKDAG 1
Torsdag 12. februar 2009, kl 10:20 - 11:05
Rococo-salen, Grand hotel
Long term Outcomes and Comorbidity. 14-Month Outcomes
Teacher SNAP-Inattention
Parent SNAP-Hyp/Impulsive
Lessons from the MTA-study
3 3
CC
T im e x T x : F = 1 0 . 6 , p < . 0 0 0 1
T im e x T x : F = 2 1 . 5 , p < . 0 0 0 1 CC
S it e x T x : F = 0 . 9 , n s B eh
2 .5 2 .5 S it e x T x : F = 1 . 3 , n s
S it e : F = 2 . 7 , p < . 0 2 B eh
S it e : F = 4 . 4 , p < . 0 0 0 6
M ed M g t
2 2 M ed M g t
Peter Jensen, MD, PhD
C om b
C om b
1 .5 1 .5
Average
1 Score Average
1 Score
C om b, M edM gt > B eh, C C
0 .5 C om b, M edM gt > B eh, C C 0 .5
0 0
0 100 200 300 400 0 100 200 300 400
Assessment Point (Days) Assessment Point (Days)
5 6
14-Month Outcomes
…Putting Science to Work Teacher SNAP-ODD/Aggressive
Parent SSRS Internalizing Sx
3 CC
Long Term Outcomes of ADHD:
T im e x T x : F = 9 . 2 , p < . 0 0 0 1
T im e x T x : F = 6 . 5 , p < . 0 0 0 3 CC
B eh 1 .4
S it e x T x : F = 1 . 1 , n s
S it e x T x : F = 1 . 2 , n s B eh
2 .5
Findings from the MTA Study
S it e : F = 2 . 3 , p < . 0 5
S it e : F = 4 . 2 , p < . 0 0 1 M ed M g t
1 .2 M ed M g t
Long-term Outcomes of Childhood ADHD : 2 C om b
C om b
Lessons from the MTA Study 1 .5
1
Peter S. Jensen, MD
Average Score Average
0 .8 Score
The REACH Institute Peter S. Jensen, MD 1
Resource for Advancing Children’s Health
C om b > B eh, C C
0 .5 0 .6
C om b, M edM gt > C C
0 0 .4
The REsource for Advancing Children �
s Health
0 100 200 300 400 0 100 200 300 400
2008 Assessment Point (Days) Assessment Point (Days)
www.TheReachInstitute.org
7 8
Month
0 14 24 36
Parent-Child Arguing
14-Month Outcomes
10-m Follow-
up After
22-m Follow-
up After
MTA Study - Behavioral Treatment (Beh
(Beh)) Teacher SSRS Social Skills
14-m Treatment Stage Treatment Treatment
(MTA Cooperative Group, 1999) 3 1 .5 CC
Medication Only T im e x T x : F = 5 . 6 , p < . 0 0 0 8 CC
T im e x T x : F = 6 . 1 , p < . 0 0 0 4
144 Subjects 2 .9
S it e x T x : F = 1 . 0 , n s 1 .4 S it e x T x : F = 0 . 5 , n s B eh
Random
Psychosocial (Behavioral)
Prnt Tng Weekly 3x/month 2x/month -> monthly
2 .8 S it e : F = 2 . 8 , p < . 0 2
B eh
S it e : F = 3 . 9 , p < . 0 0 2
Assignment 1 .3 M ed M g t
Recruitment Treatment Only 2 .7 M ed M g t
Screening 144 Subjects
Diagnosis 2 .6 1 .2 C om b
C om b
579 ADHD Combined Medication and Daily
Subjects Psychosocial Treatment DRC 2 .5 1 .1
145 Subjects
2 .4
Assessment and Referral 2x/month
Average Score Average
1 Score
Tchr Cons. 2x/month By phone 2 .3
(Community Control)
No Treatment from Study; 0 .9
Assessed for 24 mo. 2 .2
C om b, B eh > C C C om b, M edM gt > C C
146 Subjects
Aide STP & Paraprof. 2 .1 0 .8
Tng counselors Aide (PPA)
Baseline Early Mid- End Follow-up Follow-up Cont. Mgt 2
0 .7
Treatment Treatment Treatment (24 m) (36 m) 0 100 200 300 400 0 100 200 300 400
(3 m) (9 m) (14 m) Recruitment of Spring | Summer | Fall | Winter | Spring Assessment Point (Days)
LNCG Cohort Assessment Point (Days)
Assessment Points 3 4 9 10
14 NK 15 NK% “Normalized”
Normalized” at 14-month Endpoint
Teacher-Rated Inattention Public Assistance/Welfare as a Moderator: MTA Study - 14 Month Outcomes
(CC Children Separated By Med Use) Teacher Social Skills; On Assistance
MTA Groups vs. Classroom Controls Summary 1
2.5
100
88% T im e x T x : F = 2 1 .5 , p < .0 0 0 1 For children age 7-10 with ADHD
Key Differences,
80 MedMgt vs. CC:
S ite x T x : F = 0 .6 , n s
(combined type), well-delivered
68%
medication is superior to Beh Mgt and
2 C C -N o S ite : F = 2 .5 , p < .0 4
M e ds
56%
C l a s s C n tr l s
Initial Titration
60
C o m b
C C -M e ds may be sufficient for ADHD symptoms
M ed M g t Dose 1.5
CC
40 34% Beh
Average Score
25% Dose Frequency Behavioral management is an acceptable
B eh BEH
Average Score Med
20 C o m C a re 1
treatment for those preferring not to use
MED
#Visits/year M ed x C om b
medication
Comb M ed x B eh COMB
0
B a s e l in e E n d p o in t Length of Visits 0.5
M ed x C C
0 100 200 300 400
MTA N = 579 Contact w/schools A s s e s s m e n t P o in t ( D a y s ) Assessment Point (Days)
Classroom Cntrls N = 288
1 17 18
Anxiety Comorbidity as an Moderator: MTA Study - 14 Month Outcomes MTA Study - 14 Month Outcomes
Parent-Inattention, No Baseline Anxiety
3
Summary 2 Summary 3
2 .5 For some outcomes other than ADHD, the combination For some subgroups of children, the
of medication and behavioral management may be
“Comorbidity- as-a-Moderator
as-a-Moderator”” of 2 preferable: combination of medication and behavioral
Outcomes:
CC
-- parent-child conflict management may be preferable (for some
outcomes):
B eh
1 .5 -- academic difficulties
M ed -- social skills
-- anxiety symptoms
14-month Findings Average Score
1 C om b
-- oppositional/aggressive symptoms -- Children with Anxiety disorders
0 .5 IT T : C om b, M ed > B eh, C C
-- consumer satisfaction
-- Children with high levels of socio-economic
0
and/or family stressors
0 100 200 300 400 500
Assessment Point (Days)
13 14 19 20
Anxiety Comorbidity as an Moderator: Public Assistance/Welfare as a Moderator: Co-Occurring Disorders in MTA Children
Parent-Inattention, With Baseline Anxiety Teacher Social Skills; Not On Assistance (n=579) Parent SNAP Treatment Response (n=579
(n=579))
By Comorbidity Group
3
T im e x T x x A n x : F = 2 . 3 , p < . 0 8
T im e x T x : F = 1 7 . 3 , p < . 0 0 0 1
2 .5
S it e x T x : F = 0 . 5 , n s
1
S it e : F = 2 . 5 , p < . 0 3 A D H D a lo n e
31%
O p p o s it io n a l
2
CC CC 0 .8
D e f ia n t D is o r d e r
B eh BEH 40% 0 .6
1 .5 T ic
M ed M g t MED
D is .
11% B eh
0 .4
Average
1 Score C om b Average Score CO MB M edM gt
B eh x M ed 0 .2 Comb
IT T : C o m b > B e h > C C M o o d
0 .5
B eh x C C M ed > C C
C o n d u c t
D is . 4% 0
D is o r d e r
14% A n x ie ty
34% - 0 .2
A D H D - o n ly w /A n x w /D B D B o th
0 D is o r d e r
0 100 200 300 400 500 - 0 .4
Assessment Point (Days) Assessment Point (Days)
Jensen et al., 2001, for the MTA Cooperative Group
15 16 21 22
16 NK 17 NKMTA Cooperative
Long Term Stimulant Effects
Tx Group
0
Group, Owens et al.,
MedMgt/Comb
X2 = 59.52***
k = .32
Beh/CC
Overall Functioning at 8 Years
2003 N=289, 178 ER N=290, 86 ER • We do know:
62% ER 30% ER
• MTA children doing better overall than at treatment entry, but – Stimulants ↓ ADHD symptoms 24 months
0 0
Par
0 Dep functioning worse than LNCG on 19/22 variables. – well-managed stimulant treatments benefit associated symptoms (ODD Sx, p-c
X2 = 15.71*** relations, social functioning, anxiety)
Ge 9 k = .23
Le 8
N=193, 133 ER
• Overall pattern:
N=91, 41 ER – ES for ADHD Sx > ES for associated functioning
45% ER
69% ER – absence of treatment group differences based on original random
Longer-term Outcomes assignment; – modest advantages of combined Meds & Beh, more pronounced for some
Severity Severity
children than others
0 0
X2 = 9.26**, k = .31 X2 = 9.09**, k = .18 – absence of associations with self-selected medication treatment
Ge 2.33
N=42, 12 ER
Lt 2.33
N=49, 29 ER
Ge 2.63
N=22, 9 ER
Lt 2.63
N=171, 124 ER • 8 Year functioning best if in Class 2 at 36 Months • We do not know:
29%
0
ER 59% ER
0
41% ER
0
73% ER
0
– Mean duration and quality of treatment in population
Group B Group D Group A – Whether stimulants remain effective even longer-term (>24 mo)
IQ
– Long-term stimulant effects on long-term outcomes? Height? Weight?
0
X2 = 7.00**, k = .37
Le 99 Ge 100
Development? Sensitization?
ER = excellent responders Par Dep = parent BDI score
N=20, 2 ER N=21, 10 ER
Le = less than or equal to Severity = child SNAP ADHD score
10%0ER 48% ER
0 Ge = greater than or equal to IQ = child Full-Scale IQ
Lt - less than
Group E Group C Gt - greater than
8-year Outcomes
GMM-defined Latent Classes of ADHD Sxs Latent classes vs. Classroom Controls General Considerations First Steps: Discussion with
(Swanson et al 2007a)
3.0
SNAP Parent Inattention
3.0
SNAP Parent Hyperactive/Impulsive
3.0
SNAP Parent ODD
• Every child diagnosed appropriately with ADHD deserves consideration of
Child and Family
an adequate trial of stimulant medications
2.5 2.5 2.5
2.0 2.0 2.0
– Stimulants work in up to 90% of children
Class 3, n= 81 (14%)
1.5
1.5 1.5
1.0
SNAP Inattention 1.0
SNAP ODD
1.0
– Most effective psychiatric treatment in childhood • Determine target behaviors of concern to family and child
Class 1, n=199 (34%) 0.5 SNAP Hyperactive/Impulsive
0.5
0.5
• Medication must be titrated; this requires close follow-up & clarity re: with input from teacher report
0.0
effects you want to see • Explain positives and negatives of medication to the family
0.0
0 14 24 36 72 96 0.0
0 14 24 36 72 96
Class 2, n=299 (52%) Months of Study
Months of Study
0 14 24 36 72 96
• If a child does not respond to a medication, re-examine diagnosis, co-
Months of Study
Parent Aggression CIS Parent Math • Explain to child that medications are not to control behavior,
LNCG, n = 289 1.35 2.0 115
existing conditions, treatment, & adherence
but to help child with self-control and ability to focus
• If stimulant medications are not used, behavioral modification is a proven
1.30 110
1.6
1.25 105
1.20
1.2
100 therapy
CIS Math
1.15 95
Aggression 0.8
1.10 90
Class 2 had a significantly (z = 3.33, p < 0.001) greater percentage
0.4
1.05 85
of cases that had been initially assigned to Comb (62%) and
1.00 0.0 80
0 14 24 36 72 96 0 14 24 36 72 96 0 14 24 36 72 96
Months of Study Months of Study
MedMgt (55%) than to Beh (46%) and CC (45%).
Months of Study
Class 1
Class 2
Class 3
LNCG-ADHD
Diagnoses at 8 Years
MTA vs LNCG stat sign for ADHD, ODD/CD Medication Management
“Hard” Outcomes at 8 Years ADHD: Stimulant Treatment • Most common reasons for failure:
– Doses too low
– Doses too far apart
• Initiating stimulant therapy – Every child has unique response to treatment; if 1 stimulant doesn’t work, try the
– Parent education regarding value of stimulant medication others
– Treatment program that recognizes ADHD as a chronic condition • Dose most effective when titrated to amount & interval to meet child’s
– Dose titration to achieve optimal dose needs
• Start low
• Titrate to optimal effect, not just measurable effect • Titration requires balancing efficacy with side effects:
– Trial of second stimulant in patients who fail to respond to first – Teacher report for efficacy of medication at school (amount & interval)
stimulant – Parent report for side effects of medications & child-parent relations
– Regular monitoring to ensure symptoms of ADHD are optimally
managed
» Greenhill L et al., J Am Acad Child Adolesc Psychiatry 2002;41(Suppl 2):26S-49S
» American Academy of Pediatrics. Pediatrics 2001;108:1033-1044
ns
MTA vs LNCG p=.0001 MTA vs LNCG p=.0003
18 NK 19 NKDAG 1
Torsdag 12. februar 2009, kl 11:05 - 11:50
Rococo-salen, Grand hotel
Differentiating ADHD and Bipolar Disorder
Peter Jensen, MD, PhD
NOTATER
The Environment
Peter S. Jensen, MD
• Increasing frequency of bipolar diagnosis in
the young
• Increasing use of mood stabilizers in
Differentiating ADHD and Bipolar Disorder psychiatric populations (lithium,
in Childhood and Adolescence
anticonvulsants, atypical antipsychotics)
• Pressure on the pharmaceutical industry to do
Director, REACH Institute studies in children
The REsource for Advancing Children’s Health
New York, NY
Anticonvulsants Lithium
4
15 3 .5
3
10 2 .5
2
1 .5
Youths
5
1
1000 Youths 0 .5
0 0
Annual Prevalence per 1000
Annual Prevalence per1 9 8 7 1991 1996 1987 1991 1996
Medicaid Mid-Atlantic State Medicaid Midwestern State Medicaid Mid-Atlantic State Medicaid Midwestern State
Health Maintenance Organization Health Maintenance Organization
Zito et al., 2003
Zito et al., 2003
20 NK 21 NKBipolar Disorder in Children & Youth: Bipolar Disorder: DSM-IV Major Is Mania “Episodic” in Children & Youth?
Antipsychotics Depressive Episode Carlson, 1999
Big Picture Issues:
5 or more symptoms of:
10 • Depressed mood most of day by subjective report or • If “episodes ” are the hallmark of mania, and all sx of mania are
observations of others (or irritable mood in kids) supposed to occur in an “episode ”, what is an episode?
8 • Current Clinical Description • Marked diminished interest or pleasure in almost all activities all – Some sx of mania occur during a rage (increased energy, racing
or most of day, nearly every day (NED)
6
• Mania – Children vs. adults thoughts, irritability). Is this temper tantrum an “episode” or a
• Sig. weight loss (kids: not making weight gains) “rapid cycle”?
4
• Epidemiology • Insomnia or hypersomnia NED – Normal moods fluctuate. Are undulations “episodes?”
• Psychomotor agitation or retardation NED – Almost all chronic conditions, including ADHD, get better and
10002 Youths
• Treatments worse. Are variations “episodes”?
• Fatigue or loss of energy NED
• Long-term Outcomes • Feelings of worthlessness or excessive guilt NED – Children with ADHD are especially out of control in overstimulating
Annual Prevalence
0 per situations, less so in more structured situations. Is playground
• Diminished ability to think or concentrate NED
• Future Research • Recurrent thoughts of death, SI w/wo plan
behavior an “episode”?
1987 1991 1996
Significant distress and/or Impairment
Medicaid Mid-Atlantic State Medicaid Midwestern State
Not physiologic, not grief
Health Maintenance Organization
Zito et al., 2003 Courtesy of Gaye Carlson, MD
Bipolar Disorder: Clinical Description Bipolar Disorder: DSM-IV Bipolar Disorder in Children/Adolescents:
Bipolar Disorder in Children/Adolescents:
Differential Diagnosis
Epidemiology
• 1% of adolescents (14–18 yr) met criteria for BD or cyclothymia • Comorbidities
• Hotly debated - formerly thought to be ”rare” • Manic vs. Hypomania episode in one study1
– ADHD
• 5.7% of youth may experience a manic symptom without full
• Spectrum of mood disorders - similar • Bipolar I (mania + depression) manic episode (none became manic over next 4 years) – Conduct disorder
symptoms and genetic factors • Bipolar II (hypomania + depression) • ~10%–15% of adolescents with recurrent major depression will – Substance abuse/dependence
develop Bipolar I disorder2
• Classic vs. non-classic presentations • Major depressive episode • Children and young adolescents may1 – Tourette’s syndrome (TS)
• Developmental differences… – Have rapid cycling of moods – Anxiety disorders
• Bipolar “NOS” – not otherwise specified – Likely to have mixed symptoms
– PDD
• Cyclothymia
• Mixed mood states
1. Child and adolescent bipolar disorder: an update from the National Institute of
Mental Health. NIH Pub. No. 00-4778, 2000. Kusumakar V, et al. Bipolar mood disorder: diagnosis, etiology, and treatment. In:
2. Diagnostic and Statistical Manual of Mental Disorders , 4th edition. Washington Kutcher S, ed. Practical Child and Adolescent Psychopharmacology . Cambridge,
DC: American Psychiatric Association; 1994. Eng: Cambridge University Press; 2002:106–133.
Bipolar Disorder: DSM-IV Manic Bipolar Disorder: DSM-IV Manic Confound #1:
Implications
Episode Episode Symptoms Switching, cycling, disinhibition
• Distinct period of abnormally and persistently elevated, 3 (4 if irritable only) symptoms of:
expansive, irritable mood > 1 week (or requiring hospitalization) • Prospective inpatient study at Stony Brook (Carlson and Mick)
• > 3 (4 if irritable only) symptoms – Drug-induced disinhibition occurs in children • Bottom line:
• inflated self esteem/grandiosity
• Symptoms do not meet criteria for mixed episode • decreased need for sleep
– Rates are low when systematically observed ~ 8% – Although many times parents will complain about
• Mood disturbance causes marked impairment in social or • talkativeness or pressured speech
– NO DIAGNOSTIC SIGNIFICANCE their child going “off the walls” on stimulants,
• Rebound occurs in 10-30% of children: 9% had to stop because under controlled situations, that phenomenon is
occupational functioning, psychosis, or hospitalization • flight of ideas of subjective experience of racing thoughts of it
• distractibility
relatively uncommon
• Not due to physiologic effects of drugs, hypothyroid, other CSN – NO DIAGNOSTIC SIGNIFICANCE
states • increase in goal-directed activity (social, sexual, work/school) or • MTA trial: no short-term differences in stimulant response – When it occurs, it can be significant, but it is not
psychomotor agitation between children with manic symptoms (defined either on the diagnostically specific
• excessive involvement in pleasurable activities with possible DISC or on the CBCL profile) and without
painful consequences
• In addition:
– NO DIAGNOSTIC SIGNIFICANCE
– There is no evidence from at least one study that
adults with bipolar spectrum disorders had a
worse response to stimulants as children
22 NK 23 NKCo-Occurring Disorders in MTA Children Bipolar vs. ADHD in the MTA Sample
Constructing a Mania “Proxy”
Proxy” in the MTA Confound #2 -
(n=579) DISC diagnosed bipolar disorder was rare in our Symptom Sharing
DISC-Mania-Proxy sample
Children with ADHD and bipolar symptoms Mania MDD ADHD ODD Anxiety
Severe Irritability plus… responded well to methylphenidate during the
A D H D a lo n e
31% O p p o s it io n a l One additional mania symptom (happy excited, 1 month titration trial elated mood
irritability 67% low frustration touchy/ irritability
D e f ia n t D is o r d e r
40% more energy, more confident) Children with ADHD and bipolar symptoms tolerance easily
annoyed
T ic 11%
N = 58 (vs. 519 without proxy) responded similarly to the remaining ADHD hyperactivity agitation hyperactivity restlessness
D is .
subjects during the 14-month treatment agitation agitation
phase distractibility poor distractibility Difficulty in
C o nd uct
M o o d
4%
CBCL-Mania-Proxy Continue to carefully diagnose and treat
conc. concentration
D is .
flight of ideas communication
D is o r d e r
14% A n x ie t y 34%
Anxious/Depressed T-Score ≥ 70 plus… patients who have some bipolar symptoms disorders
and full ADHD, stimulants and Comb txs grandiosity
Aggressive T-Score ≥ 70
D is o r d e r
remain first choice poor judgment impulsivity
N = 56 (vs. 521 without proxy) reduced sleep insomnia trouble settling
wakes early
initial insomnia
17 18 23
Titration Trial: Titration Trial:
Confound #3:
Clam Parent Report Clam Teacher Report Implications - Manic Symptoms
Manic Symptoms = Mania
CBCL-Mania-Proxy CBCL-Mania-Proxy
• 5-10% of general population of adolescents • It is unclear what children who fall in these
Figure 10. Teacher-Rated Inattentive/Overactive Symptoms (I/O)
Figure 8. Teacher-Rated byFigure
Dose12. Teacher-Rated
Aggressive/Defiant Symptoms
Symptoms (A/D) on Mixed Subscales (I/O and A/D) by Dose
by Dose • 9-22% of child/adolescent outpatients gray areas “have” but whatever it is, it is
Figure 9. Parent-Rated Inattentive/Overactive
Figure 7.Symptoms Figure 11. Parent-Rated
(I/O)Aggressive/Defiant
Parent-Rated by Dose Symptoms Symptoms
(A/D) byonDose
Mixed Subscales (I/O and A/D) by Dose
Proxy=CBCL-Bipolar-Proxy
Proxy=CBCL-Bipolar-Proxy Proxy=CBCL-Bipolar-Proxy Proxy=CBCL-Bipolar-Proxy
difficult to treat
Proxy=CBCL-Bipolar-Proxy Proxy=CBCL-Bipolar-Proxy
• 58% of psychiatrically hospitalized children • When you get a family history of bipolar
2.4 2.4
2.4 2.4 2.4
– Hospitalized longer, more hyperactive, aggressive disorder - get a very good history about the
2.4
2.1
2.1 2.1 2.1
and learning disabled, but respond similarly to family member. It is often the same
2.1
2.1
1.8
1.8 1.8 1.8
*dose
stimulants as non “manic” hospitalized ADHD complicated and comorbid unresponsive
*dose *dose
children
1.8
1.8 *cbcl-mania-proxy
*dose
*cbcl-mania-proxy
*dose
*cbcl-mania-proxy
1.5
*dose
*cbcl-mania-proxy
1.5
1.5 1.5*cbcl-mania-proxy
*dose x cbcl-mania-proxy
1.5
*dose x cbcl-mania-proxy disorder the child has
*dose1.5
x cbcl-mania-proxy
1.2
*dose x cbcl-mania-proxy
1.2
1.2 1.2
Mixed-T
1.2
• Like psychotic symptoms, manic symptoms • One suggestion is to divide mania into
1.2
Findings: Children with CBCL mania proxy have more P-CLAM symptoms, and show greater med response than children
without CBCL mania proxy Aggr/Defiant-P
0.9 0.9
Mixed-P
Findings: Aggr/Defiant-T
0.9Children with CBCL mania proxy have
Innatt/Overact-T
without CBCL mania proxy
more 0.9
0.9T-CLAM symptoms, and show greater med response than children complicate a number of disorders without primary and secondary, or BPI/II vs. NOS
Innatt/Overact-P
0.9
0.6 0.6 0.6 0.6 0.6
CBCL-Bipolar-Proxy=No
necessarily being diagnostically specific Courtesy of Gaye Carlson, MD
0.6 CBCL-Bipolar-Proxy=No CBCL-Bipolar-Proxy=No
CBCL-Bipolar-Proxy=No 0.3 CBCL-Bipolar-Proxy=Yes
CBCL-Bipolar-Proxy=No
19 0.3 0.3 CBCL-Bipolar-Proxy=Yes 20
CBCL-Bipolar-Proxy=Yes
0.3 CBCL-Bipolar-Proxy=Yes
0.3 CBCL-Bipolar-Proxy=No CBCL-Bipolar-Proxy=Yes
0.3 CBCL-Bipolar-Proxy=Yes 0.0
0.0 0.0 0.0
0.0 15 0 20 5 10 15 20
0 5 10 15 20 0 5 10 15 0 205 10
0.0 0 5 10 15 20
Dose in Mg Dose in Mg
0 5 10 15 20 Dose in Mg Dose in Mg
Dose in Mg
Dose in Mg
14 Month Measurements 14 Month Measurements
Inattention, Parent-rated ODD/Aggression, Parent-rated Mania or ADHD? Mania or ADHD? (Cont.)
by DISC-Mania-Proxy by CBCL-Mania-Proxy
DISC-Mania-Proxy(+) DISC-Mania-Proxy(-)
DISC-Mania-Proxy(-) Symptom ADHD Bipolar
3
CC
CBCL-Mania-Proxy(+) CBCL-Mania-Proxy(-) Symptom ADHD Bipolar
3
Euphoric Can get silly—transitory, Outrageous behavior
3
2 .5
Racing thoughts During mood can be
3
B eh CC
Especially if low IQ or
rarely impairing
2 .5
B eh
2 .5
2
has LD, can be difficult tough to follow, causes
M ed M g t 2 .5
2 M ed M g t
Grandiosity Can brag—usually trying to Truly believes at the time
C om b 2
1 .5
1 .5
C om b
2
to follow interference
1 .5
1 .5
boost self-esteem in outlandish ideas Goal directed Hyperactivity is chronic Engage in elaborate
Mean Mean
1
Mean 1
Mean
Need for Some have never needed Sleeps 2+ hours less than
1
score score activity and unfocused schemes & surges of
1
0 .5 Com b, M edM gt > Beh, CC score 0 .5 C om b, M edM gt > B eh, C C score
0 0
0 .5 0 .5
Sleep much sleep; medications can usual, fully rested activity
0 100 200 300 400
0 100 2 00 30 0 4 00 0
0 100 200 300 400
0
0 100 200 300 400
interfere with sleep
Day Day Days Pressured Speech Chronic motor mouth Episodes where loud,
Days
s s
hard to interrupt,
intrusive
Findings: Children w/DISC mania proxy do not have different outcomes by treatment group than those w/o DISC mania Findings: Children w/CBCL mania proxy do not have different outcomes by treatment group than those w/o CBCL mania
proxy proxy
21 22
24 NK 25 NKMania or ADHD? (Cont.) Improving Differential Dx
Symptom ADHD Bipolar • Look for symptoms more specific to Treatment
Involvement in Quality here is Has a more planful bipolar (elevated mood, grandiosity, Algorithm
pleasurable activities “mouth and/or quality and/or clearly pressured speech & racing thoughts, for Mania/
w/ potential for body engage before deviates from social
hypersexuality) Hypomani
painful consequences frontal lobe does” norms a in
• Careful family history Children &
– Bipolar disorder in one parent = 5x odds of Adolescen
bipolar disorder in child (but still only ~5%
prevalence; LaPalme et al., 1997) ts
• Look for evidence of periodicity
36
NOTATER
Long term follow up studies
Spectrum of Pediatric Bipolar
Disorders • Classic manic depression is not a significant outcome in long term follow up
studies of children with “hyperactivity”/ADHD (see Klein/Biederman debate,
1999)
• Using Loney’s data on 75 6-12 y.o. clinic referred boys with “MBD”, Carlson
found rates of 1.3% for BP I at ages 21-23 (Carlson et al (2000)
• Cohen’s epidemiological data :1.9%/1.3% adolescent mania /mania “nos”
(n=24). Only 3 subjects met criteria at late adolescence and adulthood.
Johnson et al (2000)
• 20% of an ADHD clinic sample had manic symptoms between ages 9-13;
only 1 still had them 6 years later (1.25%). Hazell et al (2003)
BOTTOM LINE: Classic Bipolar Disorder is
not an outcome of juvenile manic symptoms
Suggested Approaches for “Manic” Symptoms Occurring in the
Comorbid ADHD Following Conditions:
ADHD + Organic PDD
+ ODD/CD/Agg + Anx/Dep + Everything Schizotypal
mood
rages disorder NOS psychosis NOS
Stimulants
Anticonvulsants
Stims Stims or ATX
Meds to Atypical antipsychotic
alone or in
Decrease alone or in combination
Stims + PBM combination
arousal
Stims+PBM Stims+PBM
Stims+PBM+AAs
Stims+PBM+AAs Stims+SSRIs
Gaye Carlson, MD
33
26 NK 27 NKDAG 1
Torsdag 12. februar 2009, kl 12:00 - 12:45
NOTATER Rococo-salen, Grand hotel
Tourette Syndrome: From one phenotype to many
Andrea Cavanna, MD, PhD
Tourette Syndrome (TS) is a developmental neuropsychiatric disorder defined by the presence of
multiple motor tics and at least one phonic tic for the duration of one year with onset before age 21
years (Robertson 2000). TS has long been considered a rare disorder, but recent epidemiological
studies have consistently shown that clinical and subclinical TS in the community is relatively
common, the prevalence figure in school-age children being around 1% (Robertson 2008). Moreover,
TS is increasingly recognized as a complex disorder with a wide spectrum of associated behaviours
that can accompany the motor and vocal tics. These include both tic-related symptoms, such as pali-
, copro- and echophenomena, and psychiatric comorbidities, such as obsessive compulsive disorder
(OCD), attention-deficit hyperactivity disorder (ADHD), affective disturbances, and impulse discontrol
(Robertson 2000; Cavanna et al 2009).
Since Georges Gilles de la Tourette originally described the disorder in 1885, emphasizing the triad of
motor tics, coprolalia, and echolalia, the phenotypic definitions of TS have changed (such as the age at
onset and the presence of distress). Although both the DSM and WHO criteria have always suggested,
and indeed stipulated, that TS is a unitary condition, a number of recent studies have added to the
growing body of evidence that TS is not a unitary pathological entity and can be disaggregated into
more homogeneous symptom components. Clinical studies employing hierarchical cluster analysis
and principal-component factor analysis techniques have shown that the phenotype of TS is much
more complicated than was previously thought and there is almost certainly clinical heterogeneity.
Specifically, in all studies that have directly examined for it, one factor has included simple motor
and phonic/vocal tics. Thus, in addition to the complex aetiology of TS with genetic heterogeneity,
it appears that the TS phenotype is also heterogeneous and not unitary as suggested by both DSM
and WHO criteria, and that one phenotype may well consist of ‘simple motor and phonic tics only’
(Cavanna et al 2009). Whether or not the various factors or phenotypes are associated with different
aetiologies has not been widely studied, and further studies examining phenotypic manifestations in
the light of presumed aetiological factors are required.
In clinical practice, it has long appeared appropriate for both prognostic and therapeutic aims to
pragmatically separate TS into types which make clinical sense, namely ‘pure’ TS (motor and phonic
tics only), ‘full blown TS’ (with tic-related symptoms) and ‘TS-plus’ (with associated behavioural
problems), originally coined by Packer (1987). Whether further factor analytic studies, along with
concomitant genetic studies, will echo these sub-divisions, is eagerly awaited.
28 NK 29 NKDAG 1
References
Torsdag 12. februar 2009, kl 12:45 - 13:30
- Cavanna AE, Servo S, Monaco F, Robertson MM. More than tics: the behavioral spectrum of Gilles
Rococo-salen, Grand hotel
de la Tourette syndrome. J Neuropsy Clin Neurosci 2009 in press.
- Robertson MM. The prevalence and epidemiology of Gilles de la Tourette syndrome. J Psychosom
Res 2008;65:461-486.
Health-related quality of life in Tourette syndrome
- Robertson MM. Tourette syndrome, associated conditions and the complexities of treatment.
Brain 2000;123:425-462.
- Packer LE. Social and educational resources for patients with Tourette syndrome. Neurol Clin
Andrea Cavanna, MD, PhD
1987;15:457-473.
TS is a chronic disorder with potentially socially disabling consequences of the symptoms and
NOTATER associated disorders (Elstner et al 2001; Bernard et al 2006; Cavanna et al 2008). Health-related
quality of life (HR-QOL) is emerging as a critical measure of the overall impact of suffering from a
medical condition and the clinical outcome, as it takes into account the patient’s own subjective view.
To date, the assessment of HR-QOL in individuals with TS has been hampered by the lack of specific
tools to assess the impact of TS on patients’ lives. A previous study involving 103 adult outpatients
recruited at the Tourette clinic, National Hospital for Neurology and Neurosurgery, London,
UK, demonstrated that HR-QOL is impaired in subjects with TS by using two generic HR-QOL
instruments, namely the QOLAS and the SF-36 (Elstner et al 2001). Generic instruments have been
used in clinical trials, as they have the advantage of allowing comparison between different disease
groups. However, these instruments have limited feasibility and acceptability in neuropsychiatric
conditions. In addition, they do not address, and are unlikely to be sensitive to, specific features
important to patients with TS, such as motor and phonic tics, repetitive behaviours, and other tic-
related symptoms. Consequently generic HR-QOL instruments are likely to underestimate health
problems in TS. On the other hand, assessments of disease severity using clinical rating scales
omit patient views about issues of importance to their health, particularly those of cognitive and
emotional functioning and the impact of dysfunction on activities of daily living (ADL). Moreover, it
has been pointed out that perception of patients’ HR-QOL by physicians and patients themselves can
easily diverge from each other, possibly resulting in significant misunderstandings.
Thus, the author’s group has recently developed and validated a new disease-specific instrument for
the assessment of HR-QOL specific for patients with TS, the Gilles de la Tourette-Quality of Life scale
(GTS-QOL) (Cavanna et al 2008). The GTS-QOL is a 27-item self-report scale developed after semi-
structured interviews with 103 TS patients (data in Elstner et al 2001), extensive literature review,
and consultation with experts in movement disorders. It is based on patient and clinician views
and psychometric analysis of data from two subsequent tests in different cohorts of patients with
TS (n=192 and n=136), where it has been shown to have good standard psychometric properties of
acceptability, reliability, and validity. Therefore the GTS-QOL is proposed as the first disease-specific
HR-QOL assessment tool for patients with TS, which has been developed with input from patients,
caregivers, clinicians, and literature review and using rigorous psychometric testing. It may be used
not only to assess HR-QOL in individual patients but also in observational and epidemiological trials,
to relate neuroimaging or pathophysiological findings to patients’ HR-QOL and, most importantly, in
longitudinal studies and trials of therapeutic interventions, along with clinical rating scales.
30 NK 31 NKDAG 1
This is particularly important as a number of new strategies – including behavioural therapies,
Torsdag 12. februar 2009, kl 14:30 - 16.00
medications, and neurosurgical procedures – are currently under consideration or in clinical trials
for the treatment of patients with TS.
Rococo-salen, Grand hotel
References Narcolepsy and Hypocretin:
- Bernard BA, Stebbins GT, Siegel S, Schultz TM, Hays C, Morrissey MJ, Leurgans S, Goetz CG. The
impact of co-morbidities on Quality of Life in Gilles de la Tourette Syndrome. Neurology 2006;66(Suppl
Neurobiology, genetics and immunology
2):A365-366.
- Cavanna AE, Schrag A, Morley D, Orth M, Robertson MM, Joyce E, Critchley HD, Selai C. The Gilles
de la Tourette syndrome-Quality of Life scale (GTS-QOL): development and validation. Neurology
Emmanuel Mignot, MD, PhD
2008;71:1410-1416.
- Elstner K, Selai CE, Trimble MR, Robertson MM. Quality of Life (QOL) of patients with Gilles de la
Tourette’s syndrome. Acta Psychiatrica Scand 2001;103:52-59.
NOTATER Emmanuel Mignot, Lior Appelbaum, Juliette Faraco, Ling Lin, Philippe Mourrain, Tohei Yokogawa,
Shengwen Zhang
Howard Hughes Medical Institute, Stanford University, Palo Alto, CA, USA 94305
Human narcolepsy is genetically complex, and environmentally influenced. One of the predisposing
factors is the Human Leukocyte Antigen (HLA) DQ, and at this locus multiple allele interact to confer
various degree of susceptibility. An autoimmune mediation is suspected but unproven.
Positional cloning in a canine single gene mutant model and mouse knockout studies have shown
that the key pathway involved in the pathophysiology of the disorder is the neurotransmitter
hypocretin (orexin). A deficiency in this system mediates the symptoms of the disorder in humans,
but not through direct mutations of these genes (except in a single case). Gene expression studies
in human brains and rodent narcolepsy models have led to the identification of other candidate
molecules with preferential expression in hypocretin cells. These molecules are novel candidates for
the pathophysiology of narcolepsy, as targets for a putative autoimmune attack or as mediators of
hypocretin cellular death.
We are also using the zebrafish as a model to functionally knockdown some of these candidate
genes and study hypocretin cell physiology. The zebrafish model can also be used to screen for novel
mutation that may affect hypocretin cell development and maintenance. Together with more classical
genome-wide association studies in narcolepsy and other hypersomnia syndrome, work in animal
models is likely to assist in the discovery and functional testing of novel narcolepsy susceptibility
factors.
Studies of the hypocretin system across species are not only informative with regards to narcolepsy,
but are also shedding new light on how sleep-regulatory networks have emerged across evolution
and in relation to selected ecological niches.
Funded by the Howard Hughes Medical Institute, NS-23724 and MH080957
32 NK 33 NKDAG 1
Torsdag 12. februar 2009, kl 16:30 - 17:30
NOTATER Rococo-salen, Grand hotel
Opplæring og evidensbaserte
atferdstiltak - en oversikt
Terje Ogden, professor
Foredraget gir en oversikt over mål og innhold i utvalgte program og tiltak for barn og unge som har
problemer med å mestre skolearbeidet og tilpasse seg skolen på grunn av sin atferd. Evidensbasert
praksis stiller bestemte krav til forskning og praktisk gjennomføringen av tiltak. Kravene knytter
seg til kvaliteten av forskningsgrunnlaget, beskrivelser av programinnhold, implementering av
tiltak samt evaluering av resultater og gjennomføring. Program og tiltak kan være skolebaserte
og skoleomfattende, men også ha sin basis i familie- og nærmiljø. De skal tilpasses elevens
forutsetninger og risikonivå, og beskrives som universelle for alle elever eller selekterte og indikerte
for elever som har, eller står i fare for å utvikle atferdsproblemer. Lovende program kjennetegnes av
å legge vekt på å redusere risikofaktorer og fremme beskyttende faktorer i forhold til skolefaglige
og sosiale vansker i skolen. Målsettinger knyttes først og fremst opp til reduksjon av problematferd
og styrking av skolefaglig og sosial kompetanse. Problematferd forebygges når elever er 1) aktivt
engasjert i aktiviteter sammen med andre, 2) når det vet hva de skal gjøre, når de skal gjøre det
og hvordan de skal gjøre det, 3) når de forstår hvilke forventninger som stilles til atferden deres
og 4) når de mestrer elevrollen og har sosiale ferdigheter for å lykkes i forhold til medelever og
lærere. Innholdskomponenter omfatter blant annet funksjonsanalyse av atferd (eng. functional
assessment), positiv atferdsstøtte (eng.positive behavior support), klasseledelse (eng. classroom
management), sinnemestring (eng. anger control & aggression replacement training) og sosial
ferdighetsopplæring.
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