Executive dysfunction in early stages of Huntington's disease is associated with striatal and insular atrophy: A neuropsychological and voxel-based morphometric study

Peinemann, Alexander; Schuller, Sabine; Pohl, C.; Jähn, Thomas; Weindl, A.; Kassubek, Jan

doi:10.1016/j.jns.2005.07.007

Cited by 164 publications

(121 citation statements)

References 36 publications

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“…12,13 While most studies focused on the correlation between the subcortical and cortical GM atrophy and the genetic and clinical features, 19,22 Jech et al 37 also found a correlation between WM volume loss and both the number of abnormal triplets and the UHDRS motor score. In line with prior VBM investigations, 37,38 in our study parametric VBM analysis demonstrated significant correlation of the motor and executive function deficits with atrophy of the neostriatum and the cerebral cortex. The same deficits also correlated with multiple areas of WM atrophy, including the internal capsule, corpus callosum, and cerebellum, thus confirming and extending previous findings that were limited to the motor impairment.…”

Section: Discussionsupporting

confidence: 91%

Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study

Nave¹,

Ginestroni²,

Tessa³

et al. 2010

AJNR Am J Neuroradiol

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Section: Discussionsupporting

confidence: 91%

Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study

Nave¹,

Ginestroni²,

Tessa³

et al. 2010

AJNR Am J Neuroradiol

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“…This network is compromised in HD neurodegeneration (Hobbs et al 2010, Tabrizi et al 2011 Functional deterioration in HD is characterized by a well-known spectrum of clinical signs that impact everyday function. There is evidence that this spectrum includes a fronto-striatal pattern of cognitive decline and neuropsychiatric disturbance (Lawrence et al, 1998, Peinemann et al, 2005, Liston et al, 2006, Holl et al, 2013, Poudel et al, 2014, You et al, 2014. Our results extend this body of work by showing, for the first time, that the neuropsychiatric relevance of BOLD activity can be tracked longitudinally over a period of time relevant to the timeframe of clinical trials.…”

Section: Hdmentioning

confidence: 99%

Longitudinal changes in the fronto-striatal network are associated with executive dysfunction and behavioral dysregulation in Huntington's disease: 30 months IMAGE-HD data

Poudel

Stout

et al. 2017

Cortex

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Neuropsychiatric disturbance−particularly executive dysfunction and behavioral dysregulation−is a common feature of Huntington's disease (HD), with implications for functional capacity and quality of life. No study to date has ascertained whether longitudinal change in brain activity is associated with neuropsychiatric deficits in HD. We used a set-response-shifting task together with functional magnetic resonance imaging to investigate 30-month longitudinal blood-oxygen level dependent (BOLD) signal changes in the fronto-striatal attentional control network in premanifest and symptomatic HD (pre-HD and symp-HD, respectively), relative to healthy control participants. We also assessed the extent to which changes in the BOLD signal over time were related to neuropsychiatric measures in the domains of executive dysfunction and behavioral dysregulation.Associations were also evaluated with clinical and disease severity. We found no longitudinal BOLD differences between pre-HD and controls over 30 months. In contrast, reduction in BOLD response over time was greater in symp-HD, relative to controls, in task-related areas (e.g., anterior cingulate cortex and striatum) and in regions from the default mode network (e.g., medial prefrontal cortex and posterior cingulate/precuneus). Moreover, when considered across both premanifest and symptomatic stages, longitudinal BOLD signal decline in the right dorsolateral prefrontal cortex and putamen was associated with executive dysfunction and behavioral dysregulation measures. In addition, longitudinal reduction in BOLD signal, in fronto-striatal and default mode networks, correlated with disease severity. These results suggest that longitudinal change in fronto-striatal and default mode networks may be useful in understanding the biological underpinnings of functional decline in HD.Such findings offer new avenues for targeted treatments in terms of minimizing psychiatric impairment and potentially maximizing cognitive function.

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“…The neural substrate for this type of implicit skill learning includes areas such as SMA, pre-SMA and prefrontal cortex [34][35][36]. All these cortical areas and DLPFC are part of parallel loops that include the putamen and the caudate [37], two regions that show robust decreases of gray matter volumes in the early HD [38]. The alterations of both implicit and explicit aspects of learning could be attributed to early changes in the caudate and putamen of pHD, as suggested by Hikosaka and coworkers [34].…”

Section: Explicit and Implicit Aspects Of Motor Sequence Learning Arementioning

confidence: 99%

Implicit and explicit aspects of sequence learning in pre-symptomatic Huntington's disease

Ghilardi

Silvestri

Feigin

et al. 2008

Parkinsonism & Related Disorders

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Learning deficits may be part of the early symptoms of Huntington's disease (HD). Here we characterized implicit and explicit aspects of sequence learning in eleven pre-symptomatic HD gene carriers (pHD) and eleven normal controls. Subjects moved a cursor on a digitizing tablet and performed the following tasks: SEQ: learning to anticipate the appearance of a target sequence in two blocks; VSEQ: learning a sequence by attending to the display without moving for one block, and by moving to the sequence in a successive block (VSEQtest). Explicit learning was measured with declarative scores and number of anticipatory movements. Implicit learning was measured as a strategy change reflected in movement time. By the end of SEQ, pHD had a significantly lower number of correct anticipatory movements and lower declarative scores than controls, while in VSEQ and VSEQtest these indices improved. During all three tasks, movement time changed in controls, but not in pHD. These results suggest that both explicit and implicit aspects of sequence learning may be impaired before the onset of motor symptoms. However, when attentional demands decrease, explicit, but not implicit, learning may improve.

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Executive dysfunction in early stages of Huntington's disease is associated with striatal and insular atrophy: A neuropsychological and voxel-based morphometric study

Cited by 164 publications

References 36 publications

Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study

Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study

Longitudinal changes in the fronto-striatal network are associated with executive dysfunction and behavioral dysregulation in Huntington's disease: 30 months IMAGE-HD data

Implicit and explicit aspects of sequence learning in pre-symptomatic Huntington's disease

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