ライフサイエンスコーパス: paralimbic

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 ior default mode network, F) fronto-temporal/paralimbic and G) sensorimotor networks.

7 ed with a 'signature' of cortical atrophy in paralimbic and heteromodal association regions measured

8 Developmental abnormalities of anterior paralimbic and heteromodal frontal cortices, key structu

9 However, paralimbic and limbic activations were more prominent in

10 halamus and insular cortex and in additional paralimbic and limbic areas (orbitofrontal cortex, anter

11 ugal processing are occupied by heteromodal, paralimbic and limbic cortices, collectively known as tr

12 abilities have youthful brain regions in key paralimbic and limbic nodes of the default mode and sali

13 unimodal, downstream unimodal, heteromodal, paralimbic and limbic zones of the cerebral cortex.

14 identified starting in frontotemporal limbic/paralimbic and neocortical regions (phase I).

15 est that altered function of limbic/anterior paralimbic and prefrontal circuits in depression is acce

16 The results of this study indicate that paralimbic and sensory association areas are critically

17 of the brain, including the centrencephalic, paralimbic and unimodal sensory regions, with the specif

18 al, (C) meso/paralimbic, (D) fronto-temporal/paralimbic, and (E) sensory-motor.

19 changes in midbrain, pons, thalamus, limbic, paralimbic, and insular regions.

20 attern of brain activity changes in frontal, paralimbic, and limbic brain structures.

21 nnectivity of the amygdala with subcortical, paralimbic, and limbic structures, polymodal association

22 atter reduction involving prefrontal cortex, paralimbic, and limbic structures.

23 rved over 12 months, and activity in limbic, paralimbic, and pontine regions decreased.

24 g-related activation of a network of limbic, paralimbic, and striatal brain regions, including struct

25 th control conditions in right-sided limbic, paralimbic, and visual areas; decreases were found in le

26 riaqueductal gray), hypothalamus, limbic and paralimbic areas (amygdala and periamygdalar region) cin

27 nappropriate response tendencies) and limbic/paralimbic areas (commonly associated with the regulatio

28 reases in rCBF in the vicinity of the limbic/paralimbic areas (i.e., hippocampal formation, temporal

29 izophrenia and suggest the importance of the paralimbic areas and their connections with prefrontal b

30 Overall, these data posit mGluR5 in key paralimbic areas as a strong determinant of the temperam

31 ns of mesencephalon, diencephalon and limbic/paralimbic areas involved in primal emotions engendered

32 We identified a brain network of paralimbic areas such as anterior cingulate and insular

33 ulated functional connectivity of limbic and paralimbic areas such as the amygdala and insula.

34 greater activation in the frontotemporal and paralimbic areas than did the women (P < 0.005).

35 as with strong reciprocal connections to the paralimbic areas that were volumetrically reduced.

36 endent changes in the activity of limbic and paralimbic areas, including the insula, cingulate and me

37 rCBF decreases in limbic/paralimbic areas, temporal and occipital cortex, and cer

38 lume of the hippocampus and other limbic and paralimbic areas.

39 tal cortex and other prefrontal, limbic, and paralimbic areas.

40 With sadness, increases in limbic-paralimbic blood flow (subgenual cingulate, anterior ins

41 associated with changes in a discrete limbic-paralimbic brain network, representing a neural mechanis

42 y comparing the thickness of neocortical and paralimbic brain regions between cocaine-dependent and m

43 ed a distributed network of primarily limbic/paralimbic brain regions, including multiple foci in dor

44 t sizes were in the middle frontal gyrus and paralimbic brain regions, such as the frontomedial and f

45 d with increases in blood flow in limbic and paralimbic brain structures.

46 Procaine increased anterior paralimbic CBF, and different clinical responses appeare

47 lobal CBF and, to a greater extent, anterior paralimbic CBF.

48 The paralimbic circuit (C-D), which uniquely distinguished b

49 studies implicate dysfunction of limbic and paralimbic circuitry, including the amygdala and medial

50 lated sensorimotor, language, executive, and paralimbic circuits identified in this study may account

51 sponses appear to be regulated by limbic and paralimbic circuits.

52 arily mediated by an interaction between the paralimbic cortex (i.e., orbitofrontal, cingulate, insul

53 in both the maturation of the olfactocentric paralimbic cortex and in the emergence of bipolar disord

54 that REM sleep activates limbic and anterior paralimbic cortex and that depressed patients demonstrat

55 ave differences in cortical thickness in the paralimbic cortex and whether potential differences are

56 phological development of the olfactocentric paralimbic cortex has received little study.

57 licate a central role for the olfactocentric paralimbic cortex in the development of bipolar disorder

58 ties in the morphology of the olfactocentric paralimbic cortex may contribute to the bipolar disorder

59 ne use, may reflect a primary deficit in the paralimbic cortex or in its mesolimbic input.

60 The olfactocentric paralimbic cortex plays a critical role in the regulatio

61 ypothesis that differences in olfactocentric paralimbic cortex structure are a morphological feature

62 ifferences in mean cortical thickness of the paralimbic cortex were measured by using FreeSurfer soft

63 with the midbrain dopamine system, including paralimbic cortex, are preferentially activated by decis

64 m nucleus, temporal cortex, piriform cortex, paralimbic cortex, hippocampus, subiculum, entorhinal co

65 ith a weakened expected reward signal in the paralimbic cortex,which in turn predicted the behavioral

66 o study electromagnetic signaling in deeper, paralimbic cortical structures such as the medial prefro

67 atter deficits in the cingulate, limbic, and paralimbic cortices of MA abusers (averaging 11.3% below

68 Limbic and paralimbic cortices of the brain receive the heaviest ch

69 tical work, that dorsolateral prefrontal and paralimbic cortices would be significantly volumetricall

70 ance in addicts also correlated with thinner paralimbic cortices.

71 e tau neuropathology may originate in limbic/paralimbic cortices.

72 ) anterior default mode/prefrontal, (C) meso/paralimbic, (D) fronto-temporal/paralimbic, and (E) sens

73 These findings, together with the pattern of paralimbic dysfunction demonstrated among children with

74 , C) frontal/thalamic/basal ganglia, D) meso/paralimbic, E) posterior default mode network, F) fronto

75 ical glucose metabolism increases and limbic-paralimbic metabolism decreases in placebo and fluoxetin

76 t theories of abnormalities in orbitofrontal-paralimbic motivation networks in individuals with condu

77 cture modulates brain activity at the limbic-paralimbic-neocortical network (LPNN) and the default mo

78 stimulation evokes deactivation of a limbic-paralimbic-neocortical network (LPNN) as well as activat

79 buted this to changes in the activity of the paralimbic network: Pathological gamblers had reduced sy

80 clusters of lower GMV involving a limbic and paralimbic (p < .001, family-wise error [FWE] corrected)

81 ivity may index cortical activity induced by paralimbic processes involved in disinhibiting impulsive

82 where visual association cortices and their paralimbic projections may operate as a closed system di

83 n the schizophrenia group than the posterior paralimbic region.

84 sed functional cerebral activation of limbic/paralimbic regions (amygdala, ventral hippocampus, insul

85 aled that patients failed to activate limbic/paralimbic regions (eg, insular cortex, nucleus accumben

86 in limbic (the amygdala and hippocampus) and paralimbic regions (ventromedial prefrontal cortex) asso

87 en relative glucose metabolism in limbic and paralimbic regions and self-reports of depression and an

88 f structural abnormalities in olfactocentric paralimbic regions and their associated abnormalities in

89 u pathology markers in frontotemporal limbic/paralimbic regions compared to neocortical regions.

90 During pain, decreases in limbic and paralimbic regions most strongly predicted placebo analg

91 the gray matter volumes of 2 olfactocentric paralimbic regions of interest, the insular cortex and t

92 was to determine whether anterior limbic and paralimbic regions of the brain are differentially activ

93 panied by regional CBF increases in anterior paralimbic regions of the brain in trauma-exposed indivi

94 duct disorder showed decreased activation in paralimbic regions of the insula, hippocampus, and anter

95 The striking response of limbic and paralimbic regions points to these structures having a s

96 butions of the amygdala and other limbic and paralimbic regions to emotional processing, we exposed h

97 lization, in phylogenetically old limbic and paralimbic regions which include the lateral hypothalami

98 ed with concomitant activation of limbic and paralimbic regions, but with a marked reduction of activ

99 gnificant volume decreases in olfactocentric paralimbic regions, including orbitofrontal, insular and

100 ng with its tight connectivity to limbic and paralimbic regions.

101 An extended set of subcortical and paralimbic reward regions also appear to follow aspects

102 t dementia.CONCLUSIONS AND RELEVANCE-Altered paralimbic reward signals and impulsivity and/or careles

103 connectivity of prefrontal areas with limbic-paralimbic structures and enhanced connectivity within t

104 processing network including subcortical and paralimbic structures associated with vigilance, salienc

105 ivated regions in the sensorimotor and a few paralimbic structures can be identified during acupunctu

106 hy and depressed patients activated anterior paralimbic structures from waking to REM sleep, the spat

107 d increased activation of ventral limbic and paralimbic structures including the amygdala.

108 ion, may reflect dysregulation in limbic and paralimbic structures.

109 Paralimbic sulci exhibited a greater degree of anterior-

110 Surface curvature was greater for the arched paralimbic sulci than for those bounding occipital gyri

111 tomatic state are mediated by the limbic and paralimbic systems within the right hemisphere.

112 ent signal changes in regions within limbic, paralimbic, temporal, occipital, somatosensory and prefr