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1 mblers had higher impulsivity and functional paralimbic abnormalities, which could not be explained b
2                           Increased anterior paralimbic activation from waking to REM sleep may be re
3 al neuroimaging studies implicate limbic and paralimbic activity in emotional responses, but few stud
4 y distinguish sensory and motor regions from paralimbic and association regions: (i) genes enriched i
5 sory/motor profiles were anticorrelated with paralimbic and certain distributed association network p
6                        Predominantly temporo-paralimbic and frontal regions emerged as epicenters wit
7 ior default mode network, F) fronto-temporal/paralimbic and G) sensorimotor networks.
8 ed with a 'signature' of cortical atrophy in paralimbic and heteromodal association regions measured
9      Developmental abnormalities of anterior paralimbic and heteromodal frontal cortices, key structu
10                                     However, paralimbic and limbic activations were more prominent in
11 halamus and insular cortex and in additional paralimbic and limbic areas (orbitofrontal cortex, anter
12 ugal processing are occupied by heteromodal, paralimbic and limbic cortices, collectively known as tr
13 abilities have youthful brain regions in key paralimbic and limbic nodes of the default mode and sali
14  unimodal, downstream unimodal, heteromodal, paralimbic and limbic zones of the cerebral cortex.
15 ure, highlighting the hippocampus as well as paralimbic and medial default-mode regions as epicenters
16 identified starting in frontotemporal limbic/paralimbic and neocortical regions (phase I).
17 est that altered function of limbic/anterior paralimbic and prefrontal circuits in depression is acce
18 ion in TLE reflected increased similarity of paralimbic and primary sensory/motor regions.
19      The results of this study indicate that paralimbic and sensory association areas are critically
20 of the brain, including the centrencephalic, paralimbic and unimodal sensory regions, with the specif
21 al, (C) meso/paralimbic, (D) fronto-temporal/paralimbic, and (E) sensory-motor.
22 changes in midbrain, pons, thalamus, limbic, paralimbic, and insular regions.
23 attern of brain activity changes in frontal, paralimbic, and limbic brain structures.
24 nnectivity of the amygdala with subcortical, paralimbic, and limbic structures, polymodal association
25 atter reduction involving prefrontal cortex, paralimbic, and limbic structures.
26 rved over 12 months, and activity in limbic, paralimbic, and pontine regions decreased.
27 g-related activation of a network of limbic, paralimbic, and striatal brain regions, including struct
28 th control conditions in right-sided limbic, paralimbic, and visual areas; decreases were found in le
29 riaqueductal gray), hypothalamus, limbic and paralimbic areas (amygdala and periamygdalar region) cin
30 nappropriate response tendencies) and limbic/paralimbic areas (commonly associated with the regulatio
31 reases in rCBF in the vicinity of the limbic/paralimbic areas (i.e., hippocampal formation, temporal
32 izophrenia and suggest the importance of the paralimbic areas and their connections with prefrontal b
33      Overall, these data posit mGluR5 in key paralimbic areas as a strong determinant of the temperam
34 ns of mesencephalon, diencephalon and limbic/paralimbic areas involved in primal emotions engendered
35 o cortical thinning and myelination, whereas paralimbic areas specialized for affective and interocep
36             We identified a brain network of paralimbic areas such as anterior cingulate and insular
37 ulated functional connectivity of limbic and paralimbic areas such as the amygdala and insula.
38 greater activation in the frontotemporal and paralimbic areas than did the women (P < 0.005).
39 as with strong reciprocal connections to the paralimbic areas that were volumetrically reduced.
40 endent changes in the activity of limbic and paralimbic areas, including the insula, cingulate and me
41                     rCBF decreases in limbic/paralimbic areas, temporal and occipital cortex, and cer
42       Lastly, sex-bias is most pronounced in paralimbic areas, with low laminar complexity, which are
43 tal cortex and other prefrontal, limbic, and paralimbic areas.
44 lume of the hippocampus and other limbic and paralimbic areas.
45 is and synaptic transmission genes in limbic/paralimbic areas; (ii) locomotory behavior and neuronal
46                                In transmodal/paralimbic association areas, T1w/T2w starts at low leve
47            With sadness, increases in limbic-paralimbic blood flow (subgenual cingulate, anterior ins
48 associated with changes in a discrete limbic-paralimbic brain network, representing a neural mechanis
49 y comparing the thickness of neocortical and paralimbic brain regions between cocaine-dependent and m
50 ed a distributed network of primarily limbic/paralimbic brain regions, including multiple foci in dor
51  epilepsies, is associated with pathology of paralimbic brain regions, particularly in the mesiotempo
52 t sizes were in the middle frontal gyrus and paralimbic brain regions, such as the frontomedial and f
53 a, ventral hippocampus, and other limbic and paralimbic brain regions.
54 d with increases in blood flow in limbic and paralimbic brain structures.
55                  Procaine increased anterior paralimbic CBF, and different clinical responses appeare
56 lobal CBF and, to a greater extent, anterior paralimbic CBF.
57  occurred in limbic (amygdalar-hippocampal), paralimbic (cingulo-insular and ventromedial prefrontal)
58                                          The paralimbic circuit (C-D), which uniquely distinguished b
59  studies implicate dysfunction of limbic and paralimbic circuitry, including the amygdala and medial
60 lated sensorimotor, language, executive, and paralimbic circuits identified in this study may account
61 sponses appear to be regulated by limbic and paralimbic circuits.
62 arily mediated by an interaction between the paralimbic cortex (i.e., orbitofrontal, cingulate, insul
63 in both the maturation of the olfactocentric paralimbic cortex and in the emergence of bipolar disord
64 that REM sleep activates limbic and anterior paralimbic cortex and that depressed patients demonstrat
65 ave differences in cortical thickness in the paralimbic cortex and whether potential differences are
66 phological development of the olfactocentric paralimbic cortex has received little study.
67 licate a central role for the olfactocentric paralimbic cortex in the development of bipolar disorder
68 ties in the morphology of the olfactocentric paralimbic cortex may contribute to the bipolar disorder
69 orrelation in ventral frontal olfactocentric-paralimbic cortex of subjects with PD but not HCs.
70 ne use, may reflect a primary deficit in the paralimbic cortex or in its mesolimbic input.
71                           The olfactocentric paralimbic cortex plays a critical role in the regulatio
72 ypothesis that differences in olfactocentric paralimbic cortex structure are a morphological feature
73 ifferences in mean cortical thickness of the paralimbic cortex were measured by using FreeSurfer soft
74 with the midbrain dopamine system, including paralimbic cortex, are preferentially activated by decis
75 m nucleus, temporal cortex, piriform cortex, paralimbic cortex, hippocampus, subiculum, entorhinal co
76 ith a weakened expected reward signal in the paralimbic cortex,which in turn predicted the behavioral
77 onal impulsivity in the amygdala and frontal paralimbic cortex.
78 zontal axis from unimodal to heteromodal and paralimbic cortex; a radial axis where visual (ventral),
79 nd that morphometric similarity increased in paralimbic cortical areas, e.g., insula and cingulate co
80 o study electromagnetic signaling in deeper, paralimbic cortical structures such as the medial prefro
81 es (parahippocampal and cingulate gyrus) and paralimbic cortices (insula) regions showed a significan
82 uced microstructural differentiation between paralimbic cortices and the remaining cortex with marked
83 atter deficits in the cingulate, limbic, and paralimbic cortices of MA abusers (averaging 11.3% below
84                                   Limbic and paralimbic cortices of the brain receive the heaviest ch
85 tical work, that dorsolateral prefrontal and paralimbic cortices would be significantly volumetricall
86 e tau neuropathology may originate in limbic/paralimbic cortices.
87 ance in addicts also correlated with thinner paralimbic cortices.
88 ) anterior default mode/prefrontal, (C) meso/paralimbic, (D) fronto-temporal/paralimbic, and (E) sens
89                                       Limbic-paralimbic disturbances in patients with FND may represe
90 These findings, together with the pattern of paralimbic dysfunction demonstrated among children with
91 , C) frontal/thalamic/basal ganglia, D) meso/paralimbic, E) posterior default mode network, F) fronto
92 anisotropy of tissue [FAT]) of 16 limbic and paralimbic GM regions and measures of functional outcome
93 etween childhood maltreatment and prefrontal-paralimbic GMV by modeling main effects of maltreatment
94 p by maltreatment interactions on prefrontal-paralimbic GMV.
95 magnitude of maltreatment-related prefrontal-paralimbic gray matter volume (GMV) deficits compared to
96 here visual (ventral), auditory (dorsal) and paralimbic (medial) territories encircle temporopolar co
97  layers of ATL and spreads posteriorly along paralimbic mediodorsal and associative ventrolateral pat
98 ical glucose metabolism increases and limbic-paralimbic metabolism decreases in placebo and fluoxetin
99 t theories of abnormalities in orbitofrontal-paralimbic motivation networks in individuals with condu
100 cture modulates brain activity at the limbic-paralimbic-neocortical network (LPNN) and the default mo
101  stimulation evokes deactivation of a limbic-paralimbic-neocortical network (LPNN) as well as activat
102 buted this to changes in the activity of the paralimbic network: Pathological gamblers had reduced sy
103 ction of areas elsewhere in the language and paralimbic networks, a juxtaposition not seen in lobecto
104                        Increasing hubness of paralimbic nodes in MSNs was associated with increased s
105 clusters of lower GMV involving a limbic and paralimbic (p < .001, family-wise error [FWE] corrected)
106 ivity may index cortical activity induced by paralimbic processes involved in disinhibiting impulsive
107  where visual association cortices and their paralimbic projections may operate as a closed system di
108 nvolving the creation of the incision from a paralimbic region.
109 n the schizophrenia group than the posterior paralimbic region.
110 sed functional cerebral activation of limbic/paralimbic regions (amygdala, ventral hippocampus, insul
111 aled that patients failed to activate limbic/paralimbic regions (eg, insular cortex, nucleus accumben
112 in limbic (the amygdala and hippocampus) and paralimbic regions (ventromedial prefrontal cortex) asso
113 en relative glucose metabolism in limbic and paralimbic regions and self-reports of depression and an
114 d microarchitectural differentiation between paralimbic regions and the remaining cortex provide a st
115 f structural abnormalities in olfactocentric paralimbic regions and their associated abnormalities in
116 u pathology markers in frontotemporal limbic/paralimbic regions compared to neocortical regions.
117         During pain, decreases in limbic and paralimbic regions most strongly predicted placebo analg
118  the gray matter volumes of 2 olfactocentric paralimbic regions of interest, the insular cortex and t
119 was to determine whether anterior limbic and paralimbic regions of the brain are differentially activ
120 panied by regional CBF increases in anterior paralimbic regions of the brain in trauma-exposed indivi
121 duct disorder showed decreased activation in paralimbic regions of the insula, hippocampus, and anter
122          The striking response of limbic and paralimbic regions points to these structures having a s
123 butions of the amygdala and other limbic and paralimbic regions to emotional processing, we exposed h
124 lization, in phylogenetically old limbic and paralimbic regions which include the lateral hypothalami
125 ed with concomitant activation of limbic and paralimbic regions, but with a marked reduction of activ
126 gnificant volume decreases in olfactocentric paralimbic regions, including orbitofrontal, insular and
127                      Relative to primary and paralimbic regions, unimodal and heteromodal regions sho
128 ng with its tight connectivity to limbic and paralimbic regions.
129           An extended set of subcortical and paralimbic reward regions also appear to follow aspects
130 t dementia.CONCLUSIONS AND RELEVANCE-Altered paralimbic reward signals and impulsivity and/or careles
131 connectivity of prefrontal areas with limbic-paralimbic structures and enhanced connectivity within t
132 processing network including subcortical and paralimbic structures associated with vigilance, salienc
133 ivated regions in the sensorimotor and a few paralimbic structures can be identified during acupunctu
134 hy and depressed patients activated anterior paralimbic structures from waking to REM sleep, the spat
135 d increased activation of ventral limbic and paralimbic structures including the amygdala.
136 ion, may reflect dysregulation in limbic and paralimbic structures.
137 l dissimilarity (between the isocortical and paralimbic/subcortical modules) were related to better c
138  modules, especially between isocortical and paralimbic/subcortical modules; this developmental dissi
139                                              Paralimbic sulci exhibited a greater degree of anterior-
140 Surface curvature was greater for the arched paralimbic sulci than for those bounding occipital gyri
141 possible to infer activity in the limbic and paralimbic systems from pre-frontal EEG asymmetry.
142 tomatic state are mediated by the limbic and paralimbic systems within the right hemisphere.
143 reflects activity in parts of the limbic and paralimbic systems, the entropy of that asymmetry reflec
144 easure and monitor changes in the limbic and paralimbic systems.
145 ent signal changes in regions within limbic, paralimbic, temporal, occipital, somatosensory and prefr

 
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