Decreased tracer uptake was found at CBA in "Depression + ADHD" in the caudate nuclei ("cognitive associative striatum") at the comparison with controls, and in the bilateral putamen ("sensorimotor striatum") and thalamus at the comparison with "Depression".
It is well-established that the caudate nucleus supports cognitive function, including categorization, by utilizing reward or motivation information.
Indeed, ongoing CFC has been detected in the centromedian thalamic nucleus during cognitive task performance (Fitzgerald et al., 2013).
In this report, we showed that the monitoring signals in the caudate nucleus reflecting cognitive variables were shaped by reward modulation, as more accurate representation correlated with the most variable reward outcome.
Whereas the anterior clonal cluster displays relatively more tangential dispersion and contributes predominantly to nuclei with cognitive functions, the medial ventral posterior clonal cluster forms prominent radial arrays and contributes mostly to nuclei with sensory- or motor-related activities.
The "receiving negative feedback" condition was shown to rely on the cognitive loop [10] (including caudate nucleus and VLPFC, Figure 5).
Nonetheless, involvement of the caudate nucleus in the cognitive deficits in insomnia has also not been investigated previously.
Therefore, our findings are complementary to the aforementioned study because we showed that the caudate nucleus provides abstract cognitive monitoring signals beyond flexible reward associations.
Thus, it is tempting to speculate that attention/arousal can possibly selectively enhance cognitive representation in the caudate nucleus to provide evaluation of specific on-going behavior (i.e. to improve read out of information on the most difficult decisions).
The association of low somatosensory perception and decreased FDOPA-uptake provides direct evidence for the role of the caudate nucleus in the cognitive part of the task, being a relay node of the dorsolateral prefrontal circuit.
