% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{delCampo:137097,
author = {del Campo, Natalia and Fryer, Tim D and Hong, Young T and
Smith, Rob and Brichard, Laurent and Acosta-Cabronero, Julio
and Chamberlain, Samuel R and Tait, Roger and Izquierdo,
David and Regenthal, Ralf and Dowson, Jonathan and Suckling,
John and Baron, Jean-Claude and Aigbirhio, Franklin I and
Robbins, Trevor W and Sahakian, Barbara J and Müller,
Ulrich},
title = {{A} positron emission tomography study of nigro-striatal
dopaminergic mechanisms underlying attention: implications
for {ADHD} and its treatment.},
journal = {Brain},
volume = {136},
number = {11},
issn = {1460-2156},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DZNE-2020-03419},
pages = {3252-3270},
year = {2013},
abstract = {Through the combined use of (18)F-fallypride positron
emission tomography and magnetic resonance imaging this
study examined the neural mechanisms underlying the
attentional deficits associated with attention
deficit/hyperactivity disorder and their potential reversal
with a single therapeutic dose of methylphenidate. Sixteen
adult patients with attention deficit/hyperactivity disorder
and 16 matched healthy control subjects were positron
emission tomography and magnetic resonance imaging scanned
and tested on a computerized sustained attention task after
oral methylphenidate (0.5 mg/kg) and placebo administration
in a within-subject, double-blind, cross-over design.
Although patients with attention deficit/hyperactivity
disorder as a group showed significant attentional deficits
and reduced grey matter volume in fronto-striato-cerebellar
and limbic networks, they had equivalent D2/D3 receptor
availability and equivalent increases in endogenous dopamine
after methylphenidate treatment to that observed in healthy
control subjects. However, poor attentional performers drawn
from both the attention deficit/hyperactivity disorder and
the control groups had significantly reduced left caudate
dopamine activity. Methylphenidate significantly increased
dopamine levels in all nigro-striatal regions, thereby
normalizing dopamine levels in the left caudate in low
performers. Behaviourally, methylphenidate improved
sustained attention in a baseline performance-dependent
manner, irrespective of diagnosis. This finding was
accompanied by an equally performance-dependent effect of
the drug on dopamine release in the midbrain, whereby low
performers showed reduced dopamine release in this region.
Collectively, these findings support a dimensional model of
attentional deficits and underlying nigro-striatal
dopaminergic mechanisms of attention deficit/hyperactivity
disorder that extends into the healthy population. Moreover,
they confer midbrain dopamine autoreceptors a hitherto
neglected role in the therapeutic effects of oral
methylphenidate in attention deficit/hyperactivity disorder.
The absence of significant case-control differences in D2/D3
receptor availability (despite the observed relationships
between dopamine activity and attention) suggests that
dopamine dysregulation per se is unlikely to be the primary
cause underlying attention deficit/hyperactivity disorder
pathology in adults. This conclusion is reinforced by
evidence of neuroanatomical changes in the same set of
patients with attention deficit/hyperactivity disorder.},
keywords = {Adult / Attention Deficit Disorder with Hyperactivity: drug
therapy / Attention Deficit Disorder with Hyperactivity:
metabolism / Attention Deficit Disorder with Hyperactivity:
pathology / Attention Deficit Disorder with Hyperactivity:
physiopathology / Benzamides / Corpus Striatum: drug effects
/ Corpus Striatum: metabolism / Corpus Striatum: pathology /
Corpus Striatum: physiopathology / Cross-Over Studies /
Dopamine Uptake Inhibitors: administration $\&$ dosage /
Dopamine Uptake Inhibitors: pharmacology / Double-Blind
Method / Fluorodeoxyglucose F18 / Humans / Magnetic
Resonance Imaging: instrumentation / Magnetic Resonance
Imaging: methods / Male / Mesencephalon: drug effects /
Mesencephalon: metabolism / Mesencephalon: pathology /
Mesencephalon: physiopathology / Methylphenidate:
administration $\&$ dosage / Methylphenidate: pharmacology /
Multimodal Imaging: instrumentation / Multimodal Imaging:
methods / Positron-Emission Tomography: instrumentation /
Positron-Emission Tomography: methods / Psychiatric Status
Rating Scales / Radiopharmaceuticals / Young Adult /
Benzamides (NLM Chemicals) / Dopamine Uptake Inhibitors (NLM
Chemicals) / Radiopharmaceuticals (NLM Chemicals) /
Fluorodeoxyglucose F18 (NLM Chemicals) / Methylphenidate
(NLM Chemicals) / fallypride (NLM Chemicals)},
cin = {AG Nestor},
ddc = {610},
cid = {I:(DE-2719)1310001},
pnm = {344 - Clinical and Health Care Research (POF3-344)},
pid = {G:(DE-HGF)POF3-344},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:24163364},
pmc = {pmc:PMC4125626},
doi = {10.1093/brain/awt263},
url = {https://pub.dzne.de/record/137097},
}