Movement sequencing in Huntington disease

Georgiou‐Karistianis, Nellie; Long, Jeffrey D.; Lourens, Spencer; Stout, Julie C.; Mills, James A.; Paulsen, Jane S.

doi:10.3109/15622975.2014.895042

Cited by 14 publications

(8 citation statements)

References 55 publications

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“…Less suppression of the DMN is associated with worse performance on attention-demanding tasks. Thus, strengthened M1-PCC connectivity may be a source for disruptions in executive components of motor control in prHD, such as sequencing (Georgiou-Karistianis et al, 2014). This is compatible with the finding that a stronger M1-PCC connectivity was associated with worse performance on a measure of executive functioning (Trails B-A) and color naming (Stroop), but not motor symptoms on the UHDRS.…”

Section: Figsupporting

confidence: 79%

“…Subtle motor symptoms during the prodromal stage (ocular motor, chorea, bradykinesia, dystonia, and rigidity) are of considerable interest as the total motor symptom score on the Unified Huntington's Disease Rating Scale (UHDRS) is the most sensitive marker of disease progression, following striatal atrophy (Long et al, 2014;Paulsen et al, 2014). The performance on cognitive tasks that contain a significant motor component (e.g., movement sequencing, motor timing, circle tracing, antisaccades) also declines as proximity to diagnosis nears (Antoniades et al, 2010;Georgiou-Karistianis et al, 2014;Hinton et al, 2007;Kirkwood et al, 1999;Paulsen et al, 2004;Rowe et al, 2010;Say et al, 2011;Scahill et al, 2013). A key component of the motor network, the precentral gyrus, has emerged as a region of interest (ROI), owing to the structural and functional changes in prHD that are often associated with motor dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Functional Connectivity of Primary Motor Cortex Is Dependent on Genetic Burden in Prodromal Huntington Disease

et al. 2014

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Subtle changes in motor function have been observed in individuals with prodromal Huntington disease (prHD), but the underlying neural mechanisms are not well understood nor is the cumulative effect of the disease (disease burden) on functional connectivity. The present study examined the resting-state functional magnetic resonance imaging (rs-fMRI) connectivity of the primary motor cortex (M1) in 16 gene-negative (NEG) controls and 48 gene-positive prHD participants with various levels of disease burden. The results showed that the strength of the left M1 connectivity with the ipsilateral M1 and somatosensory areas decreased as disease burden increased and correlated with motor symptoms. Weakened M1 connectivity within the motor areas was also associated with abnormalities in long-range connections that evolved with disease burden. In this study, M1 connectivity was decreased with visual centers (bilateral cuneus), but increased with a hub of the default mode network (DMN; posterior cingulate cortex). Changes in connectivity measures were associated with worse performance on measures of cognitive-motor functioning. Short- and long-range functional connectivity disturbances were also associated with volume loss in the basal ganglia, suggesting that weakened M1 connectivity is partly a manifestation of striatal atrophy. Altogether, the results indicate that the prodromal phase of HD is associated with abnormal interhemispheric interactions among motor areas and disturbances in the connectivity of M1 with visual centers and the DMN. These changes may, respectively, contribute to increased motor symptoms, visuomotor integration problems, and deficits in the executive control of movement as individuals approach a manifest diagnosis.

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Section: Figsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Functional Connectivity of Primary Motor Cortex Is Dependent on Genetic Burden in Prodromal Huntington Disease

et al. 2014

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“…This network mediates higher level motor functions and visuospatial processing used to prepare and guide movements . Indeed, cognitive–motor control declines in prHD . SFOF architecture is compatible with the trend for a relationship between rates of change in SFOF MD and change in the TMS, which probes for oculomotor control and higher motor functions (eg, hand pronation/supination, sequencing, tandem walking).…”

Section: Discussionsupporting

confidence: 53%

Cross‐sectional and longitudinal multimodal structural imaging in prodromal Huntington's disease

et al. 2016

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Objectives Diffusivity in white-matter tracts is abnormal throughout the brain in cross-sectional studies of prodromal Huntington’s disease. To date, longitudinal changes have not been observed. The present study investigated cross-sectional and longitudinal changes in white-matter diffusivity in relationship to the phase of prodromal Huntington’s progression, and compared them with changes in brain volumes and clinical variables that track disease progression. Methods Diffusion MRI profiles were studied over two years in 37 gene-negative controls and 64 prodromal Huntington’s disease participants in varied phases of disease progression. To estimate the relative importance of diffusivity metrics in the prodromal phase, group effects were rank ordered relative to those obtained from analyses of brain volumes, motor, cognitive and sensory variables. Results First, at baseline diffusivity was abnormal throughout all tracts, especially as individuals approached a manifest Huntington’s disease diagnosis. Baseline diffusivity metrics in six tracts and basal ganglia volumes best distinguished amongst the groups. Second, group differences in longitudinal change in diffusivity were localized to the superior fronto-occipital fasciculus, most prominently in individuals closer to a diagnosis. Group differences were also observed in longitudinal changes of most brain volumes, but not clinical variables. Lastly, increases in motor symptoms across time were associated with greater changes in the superior fronto-occipital fasciculus diffusivity and corpus callosum, cerebrospinal fluid, and lateral ventricle volumes. Conclusions These novel findings provide new insights into changes within two years in different facets of brain structure and their clinical relevance to changes in symptomatology that is decisive for a manifest Huntington’s diagnosis.

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“…Efficient movements rely on both internal and external cueing; however, in the instance of HD where the basal ganglia, and subsequent internal cueing mechanism is compromised, the external cueing system must actively compensate [ 31 , 35 ]. Individuals with HD were expected to show greater reliance on the provision of external cues to guide motor performance as evidenced from previous studies [ 13 , 17 , 25 ]; however, the current findings did not support this. Movement time consistency was reduced in the cued condition, suggesting the absence of visual cues unexpectedly enhanced performance.…”

Section: Discussioncontrasting

confidence: 85%

“…In the instance of pre-HD, early striatal degeneration may result in a disruption to the timing of an action, leading to the inability to maintain consistently timed motions [ 11 , 18 , 49 , 50 ]. This has been evidenced in both simple finger tapping [ 11 , 18 ], cued sequential tapping [ 17 ], and in the more automated action of walking [ 49 , 50 ]. No study has previously investigated different kinematic components of movement during goal directed aiming.…”

Section: Introductionmentioning

confidence: 99%

Characterising Upper Limb Movements in Huntington's Disease and the Impact of Restricted Visual Cues

Jessica¹,

Ternes²,

Dimech-Betancourt³

et al. 2015

PLoS ONE

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BackgroundVoluntary motor deficits are a common feature in Huntington's disease (HD), characterised by movement slowing and performance inaccuracies. This deficit may be exacerbated when visual cues are restricted.ObjectiveTo characterize the upper limb motor profile in HD with various levels of difficulty, with and without visual targets.MethodsNine premanifest HD (pre-HD), nine early symptomatic HD (symp-HD) and nine matched controls completed a motor task incorporating Fitts' law, a model of human movement enabling the quantification of movement timing, via the manipulation of task difficulty (i.e., target size, and distance between targets). The task required participants to make reciprocal movements under cued and blind conditions. Dwell times (time stationary between movements), speed, accuracy and variability of movements were compared between groups.ResultsSymp-HD showed significantly prolonged and less consistent movement times, compared with controls and pre-HD. Furthermore, movement planning and online control were significantly impaired in symp-HD, compared with controls and pre-HD, evidenced by prolonged dwell times and deceleration times. Speed and accuracy were comparable across groups, suggesting that group differences observed in movement time, variability, dwell time and deceleration time were evident over and above simple performance measures. The presence of cues resulted in greater movement time variability in symp-HD, compared with pre-HD and controls, suggesting that the deficit in movement consistency manifested only in response to targeted movements.ConclusionsCollectively, these findings provide evidence of a deficiency in both motor planning, particularly in relation to movement timing and online control, which became exacerbated as a function of task difficulty during symp-HD stages. These variables may provide a more sensitive measure of motor dysfunction than speed and/or accuracy alone in symp-HD.

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Movement sequencing in Huntington disease

Cited by 14 publications

References 55 publications

Functional Connectivity of Primary Motor Cortex Is Dependent on Genetic Burden in Prodromal Huntington Disease

Functional Connectivity of Primary Motor Cortex Is Dependent on Genetic Burden in Prodromal Huntington Disease

Cross‐sectional and longitudinal multimodal structural imaging in prodromal Huntington's disease

Characterising Upper Limb Movements in Huntington's Disease and the Impact of Restricted Visual Cues

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