% 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{Adhikari:865828,
author = {Adhikari, Bhim M. and Dukart, Juergen and Hipp, Joerg F.
and Forsyth, Anna and McMillan, Rebecca and
Muthukumaraswamy, Suresh D. and Ryan, Meghann C. and Elliot
Hong, L. and Eickhoff, Simon and Jahanshad, Neda and
Thompson, Paul M. and Rowland, Laura M. and Kochunov, Peter},
title = {{E}ffects of {K}etamine and {M}idazolam on resting state
connectivity and comparison with {ENIGMA} connectivity
deficit patterns in schizophrenia},
journal = {Human brain mapping},
volume = {41},
number = {3},
issn = {1065-9471},
address = {New York, NY},
publisher = {Wiley-Liss},
reportid = {FZJ-2019-05119},
pages = {767-778},
year = {2020},
note = {NIH. Grant Numbers: T32MH067533, R01MH085646, R01DA027680,
R01MH112180, R01EB015611, U01MH108148, U54EB020403},
abstract = {Subanesthetic administration of ketamine is a
pharmacological model to elicit positiveand negative
symptoms of psychosis in healthy volunteers. We used resting
statepharmacological functional MRI (rsPhfMRI) to identify
cerebral networks affected by ketamineand compared them to
the functional connectivity (FC) in schizophrenia. Ketamine
can producesedation and we contrasted its effects with the
effects of the anxiolytic drug midazolam.Thirty healthy male
volunteers (age=19-37 years) underwent a randomized,
three-way,cross-over study consisting of three imaging
sessions, with 48 hours between sessions. A sessionconsisted
of a control period followed by infusion of placebo or
ketamine or midazolam. TheENIGMA rsfMRI pipeline was used to
derive two long distance (seed-based and dualregression)and
one local (regional homogeneity, ReHo) FC measures. Ketamine
inducedsignificant reductions in the connectivity of the
salience network (Cohen’s d:1.13±0.28,p=4.0×10-3),
auditory network (d: 0.67±0.26, p=0.04) and default mode
network (DMN,d:0.63±0.26, p=0.05). Midazolam significantly
reduced connectivity in the DMN (d:0.77±0.27,p=0.03). The
effect sizes for ketamine for resting networks showed a
positive correlation(r=0.59, p=0.07) with the effect sizes
for schizophrenia related deficits derived from
ENIGMA’sstudy of 261 patients and 327 controls. Effect
sizes for midazolam were not correlated with
theschizophrenia pattern (r=-0.17, p=0.65). The subtraction
of ketamine and midazolam patternsshowed a significant
positive correlation with the pattern of schizophrenia
deficits (r=0.68,p=0.03).RsPhfMRI reliably detected the
shared and divergent pharmacological actions ofketamine and
midazolam on cerebral networks. The pattern of
disconnectivity produced byketamine was positively
correlated with the pattern of connectivity deficits
observed inschizophrenia, suggesting a brain functional
basis for previously poorly understood effects of thedrug.},
cin = {INM-7},
ddc = {610},
cid = {I:(DE-Juel1)INM-7-20090406},
pnm = {573 - Neuroimaging (POF3-573) / 571 - Connectivity and
Activity (POF3-571)},
pid = {G:(DE-HGF)POF3-573 / G:(DE-HGF)POF3-571},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31633254},
UT = {WOS:000491156400001},
doi = {10.1002/hbm.24838},
url = {https://juser.fz-juelich.de/record/865828},
}