30. oktober til 1. november ble medisinstudentenes årlige forskningskonferanse, Frampeik, avholdt. De fire byene Oslo, Bergen, Trondheim og Tromsø veksler på å avholde arrangementet, og i år var det idylliske Tromsø sin tur.
Elisabet Kvadsheim, forskerlinjestudent ved UiB og medlem av KGJN, deltok på konferansen. Forskerlinjen gir medisinstudenter mulighet til å arbeide i en forskningsgruppe parallelt med studiene, og i år har Kvadsheim fulltidspermisjon for å fokusere på forskningen. Hun undersøker hvordan det autonome (ikke-viljestyrte) nervesystemet fungerer hos barn og ungdom med ADHD og angst, ved bruk av et mål kalt hjerteratevariabilitet.
Frampeik gir medisinstudenter som forsker muligheten til å presentere sine prosjekter. Det var et stort spenn i tematikken – alt fra biomarkører og medikamentutprøving til Kvadsheims forskning på ADHD. Kvadsheim fikk flere spørsmål fra salen etter presentasjonen, som kan tyde på at deltakerne syntes dette er et viktig og interessant forskningsområde.
During this year, I’ve spent two fortnights at BROAD Institute of MIT and Harvard (https://www.broadinstitute.org) to work on the genetics of ADHD. The first fortnight was in February of 2015, when I was working on the rare variant associations (exome chip content) in adult ADHD. This project is a collaborative effort within IMpACT consortium (http://www.webdesign-rijen.nl/impact/ ) led by our group at Jebsen center. The work has since been finished and we are in the process of publishing the manuscript.
The second fortnight was spent at BROAD in November 2015. This time I was working on the identification of copy number variations (CNVs) related to ADHD. Similarly to the previous project, this is a collaborative effort within Psychiatric Genomics Consortium (PGC, https://www.med.unc.edu/pgc ) that our group is leading. This is the largest CNV study in ADHD, involving over 5.000 cases and 10.000 controls. Future plans of this project involve further work at BROAD in 2016.
Kerstin J. Plessen, MD, PhD; Elena A. Allen, PhD; Heike Eichele, MD; Heidi van Wageningen, Phd; Marie Farstad Høvik, MD; Lin Sørensen, PhD; Marius Kalsås Worren, MD; Kenneth Hugdahl, PhD; Tom Eichele, MD,PhD
We examined the blood-oxygen level–dependent (BOLD) activation in brain regions that signal errors and their association with intraindividual behavioural variability and adaptation to errors in children with attention-deficit/hyperactivity disorder (ADHD).
We acquired functional MRI data during a Flanker task in medication-naive children with ADHD and healthy controls aged 8–12 years and analyzed the data using independent component analysis. For components corresponding to performance monitoring networks, we compared activations across groups and conditions and correlated them with reaction times (RT). Additionally, we analyzed post-error adaptations in behaviour and motor component activations.
We included 25 children with ADHD and 29 controls in our analysis. Children with ADHD displayed reduced activation to errors in cingulo-opercular regions and higher RT variability, but no differences of interference control. Larger BOLD amplitude to error trials significantly predicted reduced RT variability across all participants. Neither group showed evidence of post-error response slowing; however, post-error adaptation in motor networks was significantly reduced in children with ADHD. This adaptation was inversely related to activation of the right-lateralized ventral attention network (VAN) on error trials and to taskdriven connectivity between the cingulo-opercular system and the VAN.
Our study was limited by the modest sample size and imperfect matching across groups.
Our findings show a deficit in cingulo-opercular activation in children with ADHD that could relate to reduced signalling for errors. Moreover, the reduced orienting of the VAN signal may mediate deficient post-error motor adaptions. Pinpointing general performance monitoring problems to specific brain regions and operations in error processing may help to guide the targets of future treatments for ADHD.