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Aim of the project:
to investigate the role of fronto-striatal circuitry and cognitive control in
repetitive behavior in autism.
Autism is a severe childhood psychiatric disorder, which is
characterized by social and communicative deficits. Another important symptom
of autism, that has not yet received much attention in neuroimaging research,
is stereotypical and perseverative behavior.The capacity to flexibly regulate
thoughts and actions in the presence of competing ones relies on cognitive
control. This capability contributes to a wide range of complex cognitive
functions such as response inhibition, behavioral set shifting, sequence
learning and planning. A deficit in cognitive control may cause problems with
initiating appropriate behavior in unanticipated situations and result in rigid
and inflexible behavior.
Neuroimaging studies have implicated fronto-striatal
circuitry in specific aspects of cognitive control associated with the
(implicit) acquisition of sequential information as well as the ability to
adjust behavior to changing circumstances in adults and typically developing
children. Cognitive control plays a central role in research on cognitive
development, as younger children tend to be particularly susceptible to
interference of competing attentional or behavioral responses. Maturation of
cognitive control in healthy children is paralleled by a shift from diffuse to
more focal activity in fronto-striatal areas. This suggests that
fronto-striatal systems are important for the development of flexible behavior.
Recent findings in our lab show that the caudate nucleus of
the striatum is disproportionally enlarged to the rest of the brain in
medication-naïve individuals with autism. Another study found that caudate size
was positively correlated with severity of repetitive behavior. This suggests
that striatal abnormalities play a role in inflexible behavior in autism.
Several neuroimaging studies have reported deviant patterns of activity in the
prefrontal cortex and other regions associated with (intact) performance of
cognitive control tasks. It has also been shown that for different cognitive
functions (e.g. sentence comprehension, working memory and response inhibition)
individuals with autism show reduced connectivity within the cortical network
supporting cognitive performance. Together this suggests that a deficit in
cognitive control and underlying fronto-striatal circuitry may play a role in
the etiology of autism and specifically in cognitive inflexibility. In spite of
converging evidence from both structural and functional neuroimaging research
however, common fronto-striatal contributions to inflexible behavior in autism
have not yet been determined. This is possibly due to the broad definition of
cognitive control and the extended cortical network that supports different aspects
of this capability.
We hypothesize that inflexible behavior in autism may arise
as fronto-striatal systems are capable to detect implicit patterns present in
the environment but fail to detect or respond to violations of expected events.
We use fMRI to and three behavioral paradigms to address the role of the
fronto-striatal system and cognitive control in autism. The first paradigm
involves an implicit learning paradigm and is aimed at the ability to
implicitly master a recurrent pattern in a continuous stream of stimuli. The
second paradigm is a GO/NOGO task during which subjects respond to a pattern of
recurring stimuli (GO) that is violated periodically (NOGO) requiring the rapid
adaptation of ongoing behavior. The third task involves different types of
expectancy violations in a continuous stream of stimuli that require different
behavioral adaptations. We will also include functional connectivity analyses
and diffusion tensor imaging to address decreased connectivity between the
prefrontal cortex and the striatum in autism.
Investigators:
Tamar van Raalten Sarah Durston
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