Philpott AL; Cummins TD; Bailey NW; Churchyard A; Fitzgeral d PB; Georgiou-Karistianis N. Institution Philpott,April L. School of Psychological Sciences and Monash In stitute of Cognitive and Clinical Neurosciences, Monash University, Clayton, VIC, Australia. Cummins,Tarrant D R. School of Psychological Sciences and Monas h Institute of Cognitive and Clinical Neurosciences, Monash University, Clayton, VIC, Australia. Bailey,Neil W. Monash Alfred Psychiatry Research Centre, Central Clinical School, Monash University and the Alfred, Melbourne, VIC, Aust ralia. Churchyard,Andrew. Department of Neurology, Monash Medical Centr e, Clayton, VIC, Australia. Fitzgerald,Paul B. Monash Alfred Psychiatry Research Centre, Centr al Clinical School, Monash University and the Alfred, Melbourne, VIC, Australia. Georgiou-Karistianis,Nellie. School of Psychological Sciences and Monash Institute of Cognitive and Clinical Neurosciences, Monash Un iversity, Clayton, VIC, Australia. Electronic address: firstname.lastname@example.org .
Cortical inhibitory deficits in premanifest and early Hun tington’s disease.
Source: Behavioural Brain Research. 296:311-7, 2016 Jan 1.
Abstract: Although progress has been made towards understanding the gro ss cortical and subcortical pathology of Huntington’s disease (HD), t here remains little understanding of the progressive pathophysiologica l changes that occur in the brain circuits underlying the disease. Tran scranial magnetic stimulation (TMS) enables investigation of the functional int egrity of cortico-subcortical pathways, yet it has not been widely ap plied in HD research to date. This study sought to characterise profiles of cortical excitability, including inhibition and facilitation, in groups of premanifest and symptomatic HD participants via the use of TMS. We also investigated the clinical, neurocognitive and psychiatric c orrelates of cortical excitability to better understand the development of ph enotypic heterogeneity. The sample comprised 16 premanifest HD, 12 early symptomatic HD and 17 healthy control participants. Singl e- and paired-pulse TMS protocols were administered to the left primary motor cortex, with surface electromyography recorded from the abducto r pollicis brevis muscle. Short-interval cortical inhibition was signi ficantly reduced in symptomatic HD, compared with premanifest HD and co ntrols, and was significantly correlated with pathological burden and n eurocognitive performance. There was also reduced long-interval cortical inhib ition in both premanifest and symptomatic HD, compared with controls , which was associated with pathological burden and psychiatric distur bances. Motor thresholds, cortical silent periods and intracortical faci litation did not differ across groups. Our results provide important new insights into pathophysiological changes in cortico-subcortical circui ts across disease stages in HD. We propose that neurophysiological measures ob tained via TMS have potential utility as endophenotypic biomarkers in HD, given their association with both pathological burden and clinical phenotype.
Copyright © 2015 Elsevier B.V. All rights reserved.
Publication Type: Journal Article. Research Support, Non-U.S. Gov’t.