NEURAL MARKERS OF DETECTING INFREQUENT VISUAL EVENTS IN ADHD
Päivi Helenius , Marja Laasonen , Laura Hokkanen , Ritva Paetau , Markku Niemivirta
1
1
2,3
2
4
5
2
Brain Research Unit, Helsinki University of Technology, Finland, Department of Psychology, Helsinki University, Finland,
3
4
Department of Phoniatrics, Helsinki University Central Hospital, Helsinki, Finland, Department of Pediatric Neurology, Helsinki
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University Central Hospital, Finland, Department of Education, Helsinki University, Finland
MEG RESULTS: MINIMUM CURRENT ESTIMATES
INTRODUCTION
A recent model of Attention Deficit Hyperactivity Disorder (ADHD) suggests a link between deficit in learning to detect regularities or irregularities in the environment and impaired behavioral adjustment (Nigg & Casey, 2005). A positive event­related potential (ERP) component peak­
ing 300­800 ms after stimulus onset (P3 or late positive component LPC) is modulated with respect to stimulus probability and it has been suggested to manifest activa­
tion occuring when the internal model of the environment is revised (Donchin & Coles, 1988). We used magnetoen­
cephalography (MEG) and ERPs to investigate the neural processes related to successful response inhibition after infrequent visual events in adults with ADHD. Control group ADHD group Control group ADHD group
target
correct
NoGo
Fig. 2. MCEs for target and correct NoGo trials during the LPC peak. The estimates were calculated for each participant and then averaged across all control and ADHD subjects using a default brain model. The brain volumes showing stronger activation to correct NoGo than target trials are indicated with white circles. METHODS
Stimuli, experimental setup and subjects
­ Arrays composed of 5 visual items (apples and animals)
­ Relative position of items randomized between stimuli
­ Display duration 150 ms
­ Stimuli presented every 2.2 s
TARGETS (83%; wolf facing a pig)
NON­TARGETS (17%; wolf not facing a pig)
target
"Avoid responding
when a wolf is not
facing a pig"
­ Around the peak of the LPC (475­575 ms), stronger activation to correct
NoGo than to target stimuli was detected in the posterior temporal cortex
* control group bilateral NoGo > target effect (p < 0.01 in both hemispheres)
* ADHD group unilateral NoGo > target effect (right p < 0.02, left p > 0.5)
"Press a button with
your right hand as
target
non­
quickly as possible
target
when you see
target
a wolf facing
a pig"
target
target
non­
target
­ 13 control participants (7 females; age 19­48 yrs, mean 29 yrs)
­ 10 ADHD adults (4 females; age 26­49 yrs, mean 35 yrs)
recruited from DyAdd­project (Adult dyslexia and attention
deficit disorder in Finland; Laasonen et al., INS 2009, poster)
MEG RESULTS: EQUIVALENT CURRENT DIPOLES
The sources active during the LPC are clustered in the temporal cortices
Timing of the temporal activation was comparable across hemispheres and subject groups; peak around 540 ms
Amplitude of the temporal activation revealed a subtle difference between the two subject groups
* the mean difference between correct NoGo and target trials across 475
and 575 ms was smaller in ADHD than in control group (p < 0.05)
Control group
left
right
CONTROLS ADHD
Reaction times (ms) mean ± SD mean ± SD t­test p
Target hits 419 ± 37 451 ± 63 ns NoGo errors 361 ± 29 398 ± 84 ns NoGo errors mean ± SD mean ± SD
% of all non­targets 29 ± 18 19 ± 14 ns
During two approximately 12­min
sessions, 3 midline EEG channels and a
whole­head MEG system were used
to record stimulus­locked signals to
targets (response, n = 560)
correct NoGos (no response, n = 112)
N2
reference AFz
µV
Fz
Fz
0 200 400 600 ms
Pz
µV
+5
10
15
LPC
µV
target
correct NoGo
+5
10
15
+5
10
0 200 400 600 ms
µV
Cz
N2
µV
+5
10
Cz +5
10
LPC
15
µV
Pz
+5
10
15
10
10
nA m
20
200 400 600 ms
after stimulus onset 10
nA m
20
10
200 400 600 ms 200 400 600 ms
after stimulus onset correct
NoGo
target
200 400 600 ms Our results show that the bilateral posterior temporal cortex contributes to the positive ERP component LPC. Activation in the temporal area was enhanced after infre­
quent NoGo stimuli associated with a successful re­
sponse inhibition. In ADHD adults, i) the LPC component in the ERPs and ii) simultaneous activation of the bilateral temporal cortices measured with MEG, were slightly devi­
ant despite their normal task performance. Previous ERP studies have also identified unusually small P3 responses in ADHD individuals (Barry, Johnstone & Clarke, 2003). The temporal cortices and the late positive components have been associated with exploration of object­related information and memory updating triggered by incoming stimuli (Karnath, 2001; Polich, 2007). To further elucidate the fuctional significance of the late positive ERP compo­
nents and associated MEG responses, future studies should determine those cognitive defects in ADHD (e.g. visual memory impairments) that are associated with ab­
normal neural activation. ­ N2, a negative deflection 390 ms after correct NoGo stimuli
­ LPC, a late positive component 530 ms after correct NoGo stimuli
* LPC was weaker in ADHD than control subjects (p < 0.004 in Pz)
reference AFz
20
CONCLUSIONS
ERP RESULTS: CHANNELS Fz, Cz AND Pz
ADHD group
20
Fig. 3. Left: The distribution of equivalent current dipoles across all participants (control individuals orange circles, ADHD individuals grey circles) in the left and right temporal cortex shown on an atlas brain. Right: Mean time course of activa­
tion averaged across subjects for target and correct NoGo trials in the left of and right temporal areas. 306­channel Elekta Neuromag
Control group
ADHD group
target
correct NoGo
References:
Fig 1. ERP responses in electrodes Fz, Cz and Pz. The responses were averaged with respect to stimulus presentation across all control (left) and ADHD (right) sub­
jects for target and correct NoGo trials.
Barry RJ, Johnstone SJ & Clarke AR (2003) Clin Neurophysiol. 114: 184­98.
Donchin E & Coles MGH (1988) Behav Brain Sci. 11: 357­427.
Karnath HO (2001) Nat Rev Neurosci. 2: 568­76.
Nigg JT & Casey BJ (2005) Develop Psychopathol. 17: 785­806.
Polich J (2007) Clin Neurophysiol.118: 2128­48.
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