Heterotypic trajectories of dimensional psychopathology across the lifespan: the case of youth-onset attention deficit/hyperactivity disorder
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Citações na Scopus
17
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
MANFRO, Arthur Gus
SANTORO, Marcos
GADELHA, Ary
PAN, Pedro Mario
BRESSAN, Rodrigo Affonseca
BRIETZKE, Elisa
TALARICO, Fernanda
BELANGERO, Sintia
Citação
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY, v.60, n.5, p.533-544, 2019
Resumo
Background Recent studies have demonstrated the existence of a distinct late-onset attention deficit/hyperactivity disorder (ADHD) trajectory. Our objective is to test if there are distinct ADHD trajectories regarding age of onset from childhood to adolescence and to compare clinical manifestations, cognitive functions and genetic risk for ADHD among distinct longitudinal groups. Method Nine hundred and twenty four children and adolescents from the community participated in the study. We compared clinical, cognitive features and genetic risk among four groups of participants: (a) childhood-limited, (b) youth-onset, (c) childhood-onset with youth persistence, and (d) community comparisons without ADHD. Symptomatic and diagnostic assessments were performed using the Development and Well-Being Behavior Assessment, the Strengths and Difficulties Questionnaire, and the Child Behavior Checklist. Cognitive functions were measured using a battery of standardized tests. Genetic risk for ADHD was calculating using summary statistics from the Psychiatric Genomics Consortium. Results Half of the adolescents (52%) with ADHD had their symptom onset in adolescence. The impairment level of this group in adolescence is similar to the persistent group. Despite not having ADHD, the youth-onset group already presented in childhood more symptoms from other domains of psychopathology, higher shared variance in psychiatric symptomatology (p-factor), school impairment, and executive dysfunctions than community comparisons. Furthermore, the youth-onset group presented lower levels of genetic risk for ADHD compared to other cases. Conclusions A significant proportion of adolescents with ADHD were youth-onset cases and presented similar impairment levels as those cases with early-onset ADHD. The presence of cognitive impairments and higher levels of clinical symptoms in the youth-onset group already at childhood speaks in favor of a heterotypic trajectory of psychopathology suggesting that youth-onset ADHD might be an artificial consequence of categorizing dimensional psychopathology into discrete diagnostic groups.
Palavras-chave
Youth-onset, executive function, cognition, polygenic risk scores, p-factor
Referências
- Achenbach T M, 2000, Pediatr Rev, V21, P265, DOI 10.1542/pir.21-8-265
- Agnew-Blais JC, 2016, JAMA PSYCHIAT, V73, P713, DOI 10.1001/jamapsychiatry.2016.0465
- American Psychiatric Association, 2013, DIAGN STAT MAN MENT
- Anttila V, 2018, SCIENCE, V360, P1313, DOI 10.1126/science.aap8757
- Bitsakou P, 2008, J NEURAL TRANSM, V115, P261, DOI 10.1007/s00702-007-0828-z
- Caspi A, 2018, AM J PSYCHIAT, V175, P831, DOI 10.1176/appi.ajp.2018.17121383
- Caspi A, 2014, CLIN PSYCHOL SCI, V2, P119, DOI 10.1177/2167702613497473
- Castellanos FX, 2015, AM J PSYCHIAT, V172, P929, DOI 10.1176/appi.ajp.2015.15070988
- Caye A, 2016, JAMA PSYCHIAT, V73, P705, DOI 10.1001/jamapsychiatry.2016.0383
- Cooper M, 2018, J CHILD PSYCHOL PSYC, V59, P1105, DOI 10.1111/jcpp.12911
- Copeland WE, 2013, J CHILD PSYCHOL PSYC, V54, P791, DOI 10.1111/jcpp.12062
- Euesden J, 2015, BIOINFORMATICS, V31, P1466, DOI 10.1093/bioinformatics/btu848
- Faraone SV, 2016, JAMA PSYCHIAT, V73, P655, DOI 10.1001/jamapsychiatry.2016.0400
- Goodman R, 2000, J CHILD PSYCHOL PSYC, V41, P645, DOI 10.1017/S0021963099005909
- Goodman R, 2000, BRIT J PSYCHIAT, V177, P534, DOI 10.1192/bjp.177.6.534
- Hamshere ML, 2013, AM J PSYCHIAT, V170, P909, DOI 10.1176/appi.ajp.2013.12081129
- Hogan AM, 2005, DEVELOPMENTAL SCI, V8, P525, DOI 10.1111/j.1467-7687.2005.00444.x
- Ivanova MY, 2007, J CLIN CHILD ADOLESC, V36, P405, DOI 10.1080/15374410701444363
- Knouse Laura E, 2005, J Atten Disord, V8, P221, DOI 10.1177/1087054705280159
- Lahey BB, 2017, WORLD PSYCHIATRY, V16, P142, DOI 10.1002/wps.20410
- Martel MM, 2017, J ABNORM PSYCHOL, V126, P137, DOI 10.1037/abn0000205
- Martin J, 2014, BIOL PSYCHIAT, V76, P664, DOI 10.1016/j.biopsych.2014.02.013
- Moffitt TE, 2015, AM J PSYCHIAT, V172, P967, DOI 10.1176/appi.ajp.2015.14101266
- Molina B., 2014, ADHD REPORT, V22, P1
- Patton GC, 2018, NATURE, V554, P458, DOI 10.1038/nature25759
- Pine DS, 2015, ANNU REV PSYCHOL, V66, P459, DOI 10.1146/annurev-psych-010814-015038
- Pingault JB, 2015, JAMA PSYCHIAT, V72, P651, DOI 10.1001/jamapsychiatry.2015.0469
- RATCLIFF R, 1988, PSYCHOL REV, V95, P385, DOI 10.1037//0033-295X.95.3.385
- Riglin L, 2016, JAMA PSYCHIAT, V73, P1285, DOI 10.1001/jamapsychiatry.2016.2817
- Salum GA, 2014, PSYCHOL MED, V44, P3189, DOI 10.1017/S0033291714000919
- Salum GA, 2014, PSYCHOL MED, V44, P617, DOI 10.1017/S0033291713000639
- Salum GA, 2015, INT J METH PSYCH RES, V24, P58, DOI 10.1002/mpr.1459
- Shevlin M, 2017, SOC PSYCH PSYCH EPID, V52, P1135, DOI 10.1007/s00127-017-1396-7
- Sibley MH, 2018, AM J PSYCHIAT, V175, P140, DOI 10.1176/appi.ajp.2017.17030298
- Sibley MH, 2012, J CONSULT CLIN PSYCH, V80, P1052, DOI 10.1037/a0029098
- Sullivan PF, 2018, AM J PSYCHIAT, V175, P15, DOI 10.1176/appi.ajp.2017.17030283
- Toplak ME, 2005, PERCEPT MOTOR SKILL, V100, P659, DOI 10.2466/PMS.100.3.659-675
- van Bork R, 2017, THEOR PSYCHOL, V27, P759, DOI 10.1177/0959354317737185
- Vandierendonck A, 2004, BRIT J PSYCHOL, V95, P57, DOI 10.1348/000712604322779460
- White CN, 2010, J MATH PSYCHOL, V54, P39, DOI 10.1016/j.jmp.2010.01.004
- Willcutt EG, 2005, BIOL PSYCHIAT, V57, P1336, DOI 10.1016/j.biopsych.2005.02.006