Pulvinar

Benarroch, Eduardo E.

doi:10.1212/wnl.0000000000001276

Cited by 129 publications

(123 citation statements)

References 98 publications

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“…Consistent with this model, reduced connectivity in preSxC9 was detected between the medial pulvinar thalamus and regions remarkably similar to those disconnected from the right frontoinsula (salience network) seed. The medial pulvinar, an association nucleus that participates in cortico-cortical interactions, helps to guide visual attention by detecting salient environmental stimuli (Benarroch, 2015). In the rhesus monkey, the medial pulvinar shows extensive connections with the insula and high order polymodal association cortex (Mufson and Mesulam, 1984), and superior temporal gyrus and sulcus, anterior and posterior cingulate and amygdala (Romanski et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Network degeneration and dysfunction in presymptomatic C9ORF72 expansion carriers

Lee

Sias

Mandelli

et al. 2017

NeuroImage: Clinical

145

174

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Hexanucleotide repeat expansions in C9ORF72 are the most common known genetic cause of familial and sporadic frontotemporal dementia and amyotrophic lateral sclerosis. Previous work has shown that patients with behavioral variant frontotemporal dementia due to C9ORF72 show salience and sensorimotor network disruptions comparable to those seen in sporadic behavioral variant frontotemporal dementia, but it remains unknown how early in the lifespan these and other changes in brain structure and function arise. To gain insights into this question, we compared 15 presymptomatic carriers (age 43.7 ± 10.2 years, nine females) to matched healthy controls. We used voxel-based morphometry to assess gray matter, diffusion tensor imaging to interrogate white matter tracts, and task-free functional MRI to probe the salience, sensorimotor, default mode, and medial pulvinar thalamus-seeded networks. We further used a retrospective chart review to ascertain psychiatric histories in carriers and their non-carrier family members. Carriers showed normal cognition and behavior despite gray matter volume and brain connectivity deficits that were apparent as early as the fourth decade of life. Gray matter volume deficits were topographically similar though less severe than those in patients with behavioral variant frontotemporal dementia due to C9ORF72, with major foci in cingulate, insula, thalamus, and striatum. Reduced white matter integrity was found in the corpus callosum, cingulum bundles, corticospinal tracts, uncinate fasciculi and inferior longitudinal fasciculi. Intrinsic connectivity deficits were detected in all four networks but most prominent in salience and medial pulvinar thalamus-seeded networks. Carrier and control groups showed comparable relationships between imaging metrics and age, suggesting that deficits emerge during early adulthood. Carriers and non-carrier family members had comparable lifetime histories of psychiatric symptoms. Taken together, the findings suggest that presymptomatic C9ORF72 expansion carriers exhibit functionally compensated brain volume and connectivity deficits that are similar, though less severe, to those reported during the symptomatic phase. The early adulthood emergence of these deficits suggests that they represent aberrant network patterning during development, an early neurodegeneration prodrome, or both.

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Section: Discussionmentioning

confidence: 99%

Network degeneration and dysfunction in presymptomatic C9ORF72 expansion carriers

Lee

Sias

Mandelli

et al. 2017

NeuroImage: Clinical

145

174

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“…Especially, the pulvinar is a key node in the visual attention network (Benarroch, 2015). Six stereological studies have investigated the pulvinar in schizophrenia (Table 4).…”

Section: Postmortem Thalamic Findings In Schizophrenia Based Upon mentioning

confidence: 99%

Postmortem structural studies of the thalamus in schizophrenia

Dorph‐Petersen

Lewis

2017

Schizophrenia Research

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In this review, we seek to answer the following question: Do findings in the current literature support the idea that thalamo-cortical dysfunction in schizophrenia is due to structural abnormalities in the thalamus? We base our review on the existing literature of design-unbiased stereological studies of the postmortem thalamus from subjects with schizophrenia. Thus, all reported results are based upon the use of unbiased principles of sampling to determine volume and/or total cell numbers of thalamus or its constituent nuclei. We found 28 such papers covering 26 studies. In a series of tables we list all positive and negative findings from the total thalamus, the mediodorsal, pulvinar and anterior nuclei, as well as less frequently studied thalamic regions. Only four studies examined the entire thalamus and the results were inconsistent. We found largely consistent evidence for structural changes (reduced volume and cell numbers) in the pulvinar located in the posterior thalamus. In contrast, findings in the mediodorsal thalamic nucleus are inconsistent, with the largest and most recent studies generally failing to support earlier reports of a lower number of neurons in schizophrenia. Thus, the current findings of stereological studies of the thalamus in schizophrenia support the idea that thalamo-cortical dysfunction in schizophrenia might be attributable, at least in part, to structural alterations in the pulvinar that could impair thalamic inputs to higher order cortical association areas in the frontal and parietal lobes. However, more studies are needed before robust conclusions can be drawn.

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“…We found that atrophy in the right pulvinar nucleus of the thalamus (and left, when we accounted for confidence ratings) was associated with lower prosocial giving. The strongest thalamic cluster was centered in the lateral portion of the right medial pulvinar nucleus (Krauth et al., 2010), an area that has strong projections to the insula and anterior cingulate cortex (Benarroch, 2015; Romanski, Giguere, Bates, & Goldman‐Rakic, 1997) and is integral for relaying incoming sensory information to distributed neural systems that support emotion and reward processing. In bvFTD, breakdown in this afferent system may interfere with generosity by hampering patients’ access to internal emotional cues that typically motivate prosocial behaviors.…”

Section: Discussionmentioning

confidence: 99%

Prosocial deficits in behavioral variant frontotemporal dementia relate to reward network atrophy

et al. 2017

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IntroductionEmpathy and shared feelings of reward motivate individuals to share resources with others when material gain is not at stake. Behavioral variant frontotemporal dementia (bvFTD) is a neurodegenerative disease that affects emotion‐ and reward‐relevant neural systems. Although there is diminished empathy and altered reward processing in bvFTD, how the disease impacts prosocial behavior is less well understood.MethodsA total of 74 participants (20 bvFTD, 15 Alzheimer's disease [AD], and 39 healthy controls) participated in this study. Inspired by token‐based paradigms from animal studies, we developed a novel task to measure prosocial giving (the “Giving Game”). On each trial of the Giving Game, participants decided how much money to offer to the experimenter, and prosocial giving was the total amount that participants gave to the experimenter when it cost them nothing to give. Voxel‐based morphometry was then used to identify brain regions that were associated with prosocial giving.ResultsProsocial giving was lower in bvFTD than in healthy controls; prosocial giving in AD did not differ significantly from either of the other groups. Whereas lower prosocial giving was associated with atrophy in the right pulvinar nucleus of the thalamus, greater prosocial giving was associated with atrophy in the left ventral striatum.ConclusionThese findings suggest that simple acts of generosity deteriorate in bvFTD due to lateralized atrophy in reward‐relevant neural systems that promote shared feelings of positive affect.

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Pulvinar

Cited by 129 publications

References 98 publications

Network degeneration and dysfunction in presymptomatic C9ORF72 expansion carriers

Network degeneration and dysfunction in presymptomatic C9ORF72 expansion carriers

Postmortem structural studies of the thalamus in schizophrenia

Prosocial deficits in behavioral variant frontotemporal dementia relate to reward network atrophy

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