The caudate: a key node in the neuronal network imbalance of insomnia?

Diederick Stoffers, Ellemarije Altena, Ysbrand D. van der Werf, Ernesto J. Sanz-Arigita, Thom A. Voorn, Rebecca G. Astill, Rob L. M. Strijers, Dé Waterman, Eus J. W. Van Someren
Brain. 2013-11-26; 137(2): 610-620
DOI: 10.1093/brain/awt329

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1. Brain. 2014 Feb;137(Pt 2):610-20. doi: 10.1093/brain/awt329. Epub 2013 Nov 26.

The caudate: a key node in the neuronal network imbalance of insomnia?

Stoffers D(1), Altena E, van der Werf YD, Sanz-Arigita EJ, Voorn TA, Astill RG,
Strijers RL, Waterman D, Van Someren EJ.

Author information:
(1)1 Department of Sleep and Cognition, Netherlands Institute for Neuroscience,
an Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam,
The Netherlands.

Insomnia is prevalent, severe and partially heritable. Unfortunately, its
neuronal correlates remain enigmatic, hampering the development of mechanistic
models and rational treatments. Consistently reported impairments concern
fragmented sleep, hyper-arousal and executive dysfunction. Because
fronto-striatal networks could well play a role in sleep, arousal regulation and
executive functioning, the present series of studies used an executive task to
evaluate fronto-striatal functioning in disturbed sleep. Patients with insomnia
showed reduced recruitment of the head of the left caudate nucleus during
executive functioning, which was not secondary to altered performance or baseline
perfusion. Individual differences in caudate recruitment were associated with
hyper-arousal severity. Seed-based functional connectivity analysis suggested
that attenuated input from a projecting orbitofrontal area with reduced grey
matter density contributes to altered caudate recruitment in patients with
insomnia. Attenuated caudate recruitment persisted after successful treatment of
insomnia, warranting evaluation as a potential vulnerability trait. A similar
selective reduction in caudate recruitment could be elicited in participants
without sleep complaints by slow-wave sleep fragmentation, providing a model to
facilitate investigation of the causes and consequences of insomnia.

DOI: 10.1093/brain/awt329
PMCID: PMC3914473
PMID: 24285642 [Indexed for MEDLINE]


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