The interaction between mood and cognitive function studied with PET
S. C. BAKER a1 , C. D. FRITH a1 and R. J. DOLAN a1
a1 Wellcome Department of Cognitive Neurology, Institute of Neurology; MRC Cyclotron Unit, Hammersmith Hospital; Royal Free Hospital School of Medicine; National Hospital for Neurology and Neurology and Neurosurgery; and University College London
Background. Experimentally induced depressed mood is a suggested model for retarded depression. We describe the neural response associated with induced mood and the locus of the interaction between systems mediating mood and cognitive function.
Methods. Normal subjects performed a verbal fluency task during induced elated and depressed mood states. Regional cerebral blood flow (rCBF) was measured as an index of neural activity using Positron Emission Tomography (PET).
Results. In both elated and depressed mood state rCBF was increased in lateral orbitofrontal cortex, rCBF was also increased in the midbrain in elated mood. In the depressed condition rCBF was decreased in rostral medial prefrontal cortex. Verbal fluency produced an expected increase of rCBF in left dorsolateral prefrontal, inferior frontal and premotor cortex, anterior cingulate and insula cortex bilaterally, the left supramarginal gyrus posteriorly and the thalamus. Activation in the verbal fluency task was attenuated throughout the left prefrontal, premotor and cingulate cortex and thalamus in both elated and depressed mood conditions. An attenuation of anterior cingulate activation was specific to depressed mood.
Conclusions. Alteration of mood is associated with activation of orbitofrontal cortex which may be critical to the experience of emotion. The mood induced modulation of verbal fluency induced activations is consistent with resting state findings of decreased function in these regions in depressed patients. The present data suggest that resting state rCBF profile may represent the modulation of spontaneous activity in this network by a core system that is dysfunctional in depression.
Address for correspondence: Professor R. J. Dolan, Wellcome Department of Cognitive Neurology, Institute of Neurology, 12 Queen Square, London WC1 3BG.