Table 1 –

Whole-brain and seed-to-voxel intrinsic connectivity distribution (ICD) findings

Whole-brain connectivity		k	p	x	y	z
Deprived Smokers > Nonsmokers
C1	L hippocampus, parahippocampus, amygdala, temporal pole, L & R cerebellum	383	.002	−30	−9	−21
C2	L & R cerebellum I-V	116	.004	24	−36	−30
C3	L cerebellum VIIIb, IX, Vllla	30	.005	−18	−54	−48
C4	L caudate	21	.005	−15	12	15
Seed-to-voxel connectivity		k	p	x	y	z
Deprived Smokers > Nonsmokers
C1	—
C2	L & R cerebellum, occipital, precuneus	2231	<.001	−21	−54	−15
C3	L & R cerebellum, occipital, brainstem	2434	<.001	18	−81	−45
C4	—
Deprived Smokers < Nonsmokers
C1	—
C2	Anterior cingulate, medial PFC	693	.002	15	39	−3
C2	R caudate, putamen, subgenual	48	.011	−24	9	48
C3	R accumbens, caudate, putamen, anterior cingulate	112	.011	18	21	0
C4	—

Whole-brain connectivity (top): Cluster descriptions, cluster size (k), peak p-values and peak MNI coordinates are shown for clusters identified in whole-brain ICD analyses of nonsmokers and smokers during deprivation. No clusters were identified as significant in whole-brain analyses comparing nonsmokers and smokers during satiation.

Seed-to-voxel connectivity (bottom): Cluster descriptions, cluster size (k), peak p-values and peak MNI coordinates are shown for clusters identified in follow-up seed-based analyses (using clusters identified in whole-brain comparisons, above) of nonsmokers and smokers during deprivation. Seed-to-voxel analyses for the left hippocampus (C1) and caudate (C4) clusters did not identify any specific regions as primary contributors whole-brain alterations, indicating that connectivity increases for these regions were diffuse in nature (i.e., not localized to a single connection).