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Grey and white matter clinico-anatomical correlates of disinhibition in neurodegenerative disease

Santillo, Alexander Frizell LU ; Lundblad, Karl; Nilsson, Markus LU ; Waldö, Maria Landqvist LU ; Van Westen, Danielle LU ; Lätt, Jimmy LU ; Nordström, Erik Blennow LU ; Vestberg, Susanna LU ; Lindberg, Olof and Nilsson, Christer LU (2016) In PLoS ONE 11(10).
Abstract

Disinhibition is an important symptom in neurodegenerative diseases. However, the clinico- anatomical underpinnings remain controversial. We explored the anatomical correlates of disinhibition in neurodegenerative disease using the perspective of grey and white matter imaging. Disinhibition was assessed with a neuropsychological test and a caregiver information- based clinical rating scale in 21 patients with prefrontal syndromes due to behavioural variant frontotemporal dementia (n = 12) or progressive supranuclear palsy (n = 9), and healthy controls (n = 25). Cortical thickness was assessed using the Freesurfer software on 3T MRI data. The integrity of selected white matter tracts was determined by the fractional anisotropy (FA) from... (More)

Disinhibition is an important symptom in neurodegenerative diseases. However, the clinico- anatomical underpinnings remain controversial. We explored the anatomical correlates of disinhibition in neurodegenerative disease using the perspective of grey and white matter imaging. Disinhibition was assessed with a neuropsychological test and a caregiver information- based clinical rating scale in 21 patients with prefrontal syndromes due to behavioural variant frontotemporal dementia (n = 12) or progressive supranuclear palsy (n = 9), and healthy controls (n = 25). Cortical thickness was assessed using the Freesurfer software on 3T MRI data. The integrity of selected white matter tracts was determined by the fractional anisotropy (FA) from Diffusion Tensor Imaging. Disinhibition correlated with the cortical thickness of the right parahippocampal gyrus, right orbitofrontal cortex and right insula and the FA of the right uncinate fasciculus and right anterior cingulum. Notably, no relationship was seen with the thickness of ventromedial prefrontal cortex. Our results support an associative model of inhibitory control, distributed in a medial temporal lobe-insularorbitofrontal network, connected by the intercommunicating white matter tracts. This reconciles some of the divergences among previous studies, but also questions the current conceptualisation of the prefrontal syndrome and the central role attributed to the ventromedial prefrontal cortex in inhibitory control.

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author
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publication status
published
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in
PLoS ONE
volume
11
issue
10
publisher
Public Library of Science
external identifiers
  • scopus:84991453718
  • wos:000385504100022
ISSN
1932-6203
DOI
10.1371/journal.pone.0164122
language
English
LU publication?
yes
id
a2e41613-3104-43f2-95cf-26adc02edfea
date added to LUP
2016-11-01 09:33:31
date last changed
2017-08-27 06:27:51
@article{a2e41613-3104-43f2-95cf-26adc02edfea,
  abstract     = {<p>Disinhibition is an important symptom in neurodegenerative diseases. However, the clinico- anatomical underpinnings remain controversial. We explored the anatomical correlates of disinhibition in neurodegenerative disease using the perspective of grey and white matter imaging. Disinhibition was assessed with a neuropsychological test and a caregiver information- based clinical rating scale in 21 patients with prefrontal syndromes due to behavioural variant frontotemporal dementia (n = 12) or progressive supranuclear palsy (n = 9), and healthy controls (n = 25). Cortical thickness was assessed using the Freesurfer software on 3T MRI data. The integrity of selected white matter tracts was determined by the fractional anisotropy (FA) from Diffusion Tensor Imaging. Disinhibition correlated with the cortical thickness of the right parahippocampal gyrus, right orbitofrontal cortex and right insula and the FA of the right uncinate fasciculus and right anterior cingulum. Notably, no relationship was seen with the thickness of ventromedial prefrontal cortex. Our results support an associative model of inhibitory control, distributed in a medial temporal lobe-insularorbitofrontal network, connected by the intercommunicating white matter tracts. This reconciles some of the divergences among previous studies, but also questions the current conceptualisation of the prefrontal syndrome and the central role attributed to the ventromedial prefrontal cortex in inhibitory control.</p>},
  articleno    = {e0164122},
  author       = {Santillo, Alexander Frizell and Lundblad, Karl and Nilsson, Markus and Waldö, Maria Landqvist and Van Westen, Danielle and Lätt, Jimmy and Nordström, Erik Blennow and Vestberg, Susanna and Lindberg, Olof and Nilsson, Christer},
  issn         = {1932-6203},
  language     = {eng},
  month        = {10},
  number       = {10},
  publisher    = {Public Library of Science},
  series       = {PLoS ONE},
  title        = {Grey and white matter clinico-anatomical correlates of disinhibition in neurodegenerative disease},
  url          = {http://dx.doi.org/10.1371/journal.pone.0164122},
  volume       = {11},
  year         = {2016},
}