Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging studyCitation formats

  • External authors:
  • I Trender-Gerhard
  • A Gerhard
  • S Handy

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Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study. / Trender-Gerhard, I; Michou, E; Gerhard, A; Craufurd, D; Handy, S; Herholz, K.

In: Gastroenterology, Vol. 31, No. 2, 01.06.2016, p. http://www.mdsabstracts.org/abstract/dysphagia-in-.

Research output: Contribution to journalMeeting Abstractpeer-review

Harvard

Trender-Gerhard, I, Michou, E, Gerhard, A, Craufurd, D, Handy, S & Herholz, K 2016, 'Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study', Gastroenterology, vol. 31, no. 2, pp. http://www.mdsabstracts.org/abstract/dysphagia-in-.

APA

Trender-Gerhard, I., Michou, E., Gerhard, A., Craufurd, D., Handy, S., & Herholz, K. (2016). Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study. Gastroenterology, 31(2), http://www.mdsabstracts.org/abstract/dysphagia-in-.

Vancouver

Trender-Gerhard I, Michou E, Gerhard A, Craufurd D, Handy S, Herholz K. Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study. Gastroenterology. 2016 Jun 1;31(2):http://www.mdsabstracts.org/abstract/dysphagia-in-.

Author

Trender-Gerhard, I ; Michou, E ; Gerhard, A ; Craufurd, D ; Handy, S ; Herholz, K. / Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study. In: Gastroenterology. 2016 ; Vol. 31, No. 2. pp. http://www.mdsabstracts.org/abstract/dysphagia-in-.

Bibtex

@article{88f6ecbb357c4aff9b70e0b1eea9c614,
title = "Dysphagia in early stage Huntington{\textquoteright}s disease (HD) – Pilot observations from a multimodal imaging study",
abstract = "Introduction: Dysphagia is present in early stage Huntington's Disease (HD) and worsens with disease progression; resulting in weight loss, aspiration pneumonia and often death. The underlying mechanisms for oropharyngeal dysphagia in HD are not well understood. Here, we assess the central neural control of swallowing in HD patients with mild dysphagia combining fluoroscopic swallowing assessments with functional [18F]fluorodeoxyglucose Positron Emission Tomography (FDG PET). Methods: Patients with a clinical diagnosis of Huntington's disease stage I-II were approached. Only patients with mild dysphagia, based on clinical assessments, videofluoroscopy (VFS) and questionnaires, were eligible. In the pilot phase of the study, we analysed the data of 7 study participants - 3 patients with early stage HD (2 male) and 4 age-matched healthy controls. Each was assessed in a randomised, cross-over 2 scan paradigm of resting condition vs water swallowing at 20-second intervals both for 20 minutes prior to PET scanning. Motion correction was applied to correct for involuntary movements. In order to compare the differences between patients and healthy controls, we calculated the scaled differences in activation during swallowing. Results: All patients presented mild swallow impairments, with an increase in pharyngeal delay time and penetration scores in liquid swallows on VFS. In contrast to controls, the patients showed relative deactivation of the frontal cortex compared to other brain regions at rest and during swallowing tasks (Figure 1) and pronounced activation in precentral cortex and anterior cingulate superior areas. Conclusions: There are differences in brain activation patterns between early stage dysphagic HD patients and healthy controls. Frontal cortex deactivation during swallowing in HD may be due to defects of the basal ganglia-thalamocortical projections, with over-compensation for swallowing (motor cortex activation). Further analysis of the dataset will allow more definitive findings in this complex neurogenic condition. (Figure Presented).",
keywords = "Huntington chorea, adult, anterior cingulate, basal ganglion, brain region, clinical article, clinical assessment, compensation, controlled study, diagnosis, dysphagia, fluorodeoxyglucose f 18, human, involuntary movement, male, motion, motor cortex, multimodal imaging, positron emission tomography, questionnaire, randomized controlled trial, rest, thalamocortical tract, water",
author = "I Trender-Gerhard and E Michou and A Gerhard and D Craufurd and S Handy and K Herholz",
year = "2016",
month = jun,
day = "1",
language = "English",
volume = "31",
pages = "http://www.mdsabstracts.org/abstract/dysphagia--in--",
journal = "Gastroenterology",
issn = "0016-5085",
publisher = "W.B. Saunders Co. Ltd",
number = "2",

}

RIS

TY - JOUR

T1 - Dysphagia in early stage Huntington’s disease (HD) – Pilot observations from a multimodal imaging study

AU - Trender-Gerhard, I

AU - Michou, E

AU - Gerhard, A

AU - Craufurd, D

AU - Handy, S

AU - Herholz, K

PY - 2016/6/1

Y1 - 2016/6/1

N2 - Introduction: Dysphagia is present in early stage Huntington's Disease (HD) and worsens with disease progression; resulting in weight loss, aspiration pneumonia and often death. The underlying mechanisms for oropharyngeal dysphagia in HD are not well understood. Here, we assess the central neural control of swallowing in HD patients with mild dysphagia combining fluoroscopic swallowing assessments with functional [18F]fluorodeoxyglucose Positron Emission Tomography (FDG PET). Methods: Patients with a clinical diagnosis of Huntington's disease stage I-II were approached. Only patients with mild dysphagia, based on clinical assessments, videofluoroscopy (VFS) and questionnaires, were eligible. In the pilot phase of the study, we analysed the data of 7 study participants - 3 patients with early stage HD (2 male) and 4 age-matched healthy controls. Each was assessed in a randomised, cross-over 2 scan paradigm of resting condition vs water swallowing at 20-second intervals both for 20 minutes prior to PET scanning. Motion correction was applied to correct for involuntary movements. In order to compare the differences between patients and healthy controls, we calculated the scaled differences in activation during swallowing. Results: All patients presented mild swallow impairments, with an increase in pharyngeal delay time and penetration scores in liquid swallows on VFS. In contrast to controls, the patients showed relative deactivation of the frontal cortex compared to other brain regions at rest and during swallowing tasks (Figure 1) and pronounced activation in precentral cortex and anterior cingulate superior areas. Conclusions: There are differences in brain activation patterns between early stage dysphagic HD patients and healthy controls. Frontal cortex deactivation during swallowing in HD may be due to defects of the basal ganglia-thalamocortical projections, with over-compensation for swallowing (motor cortex activation). Further analysis of the dataset will allow more definitive findings in this complex neurogenic condition. (Figure Presented).

AB - Introduction: Dysphagia is present in early stage Huntington's Disease (HD) and worsens with disease progression; resulting in weight loss, aspiration pneumonia and often death. The underlying mechanisms for oropharyngeal dysphagia in HD are not well understood. Here, we assess the central neural control of swallowing in HD patients with mild dysphagia combining fluoroscopic swallowing assessments with functional [18F]fluorodeoxyglucose Positron Emission Tomography (FDG PET). Methods: Patients with a clinical diagnosis of Huntington's disease stage I-II were approached. Only patients with mild dysphagia, based on clinical assessments, videofluoroscopy (VFS) and questionnaires, were eligible. In the pilot phase of the study, we analysed the data of 7 study participants - 3 patients with early stage HD (2 male) and 4 age-matched healthy controls. Each was assessed in a randomised, cross-over 2 scan paradigm of resting condition vs water swallowing at 20-second intervals both for 20 minutes prior to PET scanning. Motion correction was applied to correct for involuntary movements. In order to compare the differences between patients and healthy controls, we calculated the scaled differences in activation during swallowing. Results: All patients presented mild swallow impairments, with an increase in pharyngeal delay time and penetration scores in liquid swallows on VFS. In contrast to controls, the patients showed relative deactivation of the frontal cortex compared to other brain regions at rest and during swallowing tasks (Figure 1) and pronounced activation in precentral cortex and anterior cingulate superior areas. Conclusions: There are differences in brain activation patterns between early stage dysphagic HD patients and healthy controls. Frontal cortex deactivation during swallowing in HD may be due to defects of the basal ganglia-thalamocortical projections, with over-compensation for swallowing (motor cortex activation). Further analysis of the dataset will allow more definitive findings in this complex neurogenic condition. (Figure Presented).

KW - Huntington chorea

KW - adult

KW - anterior cingulate

KW - basal ganglion

KW - brain region

KW - clinical article

KW - clinical assessment

KW - compensation

KW - controlled study

KW - diagnosis

KW - dysphagia

KW - fluorodeoxyglucose f 18

KW - human

KW - involuntary movement

KW - male

KW - motion

KW - motor cortex

KW - multimodal imaging

KW - positron emission tomography

KW - questionnaire

KW - randomized controlled trial

KW - rest

KW - thalamocortical tract

KW - water

UR - https://insights.ovid.com/movement-disorders/mdis/2016/06/002/dysphagia-early-stage-huntington-disease-hd-pilot/1114/01445483

M3 - Meeting Abstract

VL - 31

SP - http://www.mdsabstracts.org/abstract/dysphagia-in-

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 2

ER -