title: Altered cortico-basal ganglia motor pathways reflect reduced volitional motor activity in schizophrenia.
abstract: Little is known about the neurobiology of hypokinesia in schizophrenia. Therefore, the aim of this study was to investigate alterations of white matter motor pathways in schizophrenia and to relate our findings to objectively measured motor activity. We examined 21 schizophrenia patients and 21 healthy controls using diffusion tensor imaging and actigraphy. We applied a probabilistic fibre tracking approach to investigate pathways connecting the dorsolateral prefrontal cortex (dlPFC), the rostral anterior cingulate cortex (rACC), the pre-supplementary motor area (pre-SMA), the supplementary motor area proper (SMA-proper), the primary motor cortex (M1), the caudate nucleus, the striatum, the pallidum and the thalamus. Schizophrenia patients had lower activity levels than controls. In schizophrenia we found higher probability indices forming part of a bundle of interest (PIBI) in pathways connecting rACC, pre-SMA and SMA-proper as well as in pathways connecting M1 and pre-SMA with caudate nucleus, putamen, pallidum and thalamus and a reduced spatial extension of motor pathways in schizophrenia. There was a positive correlation between PIBI and activity level in the right pre-SMA-pallidum and the left M1-thalamus connection in healthy controls, and in the left pre-SMA-SMA-proper pathway in schizophrenia. Our results point to reduced volitional motor activity and altered motor pathway organisation in schizophrenia. The identified associations between the amount of movement and structural connectivity of motor pathways suggest dysfunction of cortico-basal ganglia pathways in the pathophysiology of hypokinesia in schizophrenia. Schizophrenia patients may use cortical pathways involving the supplementary motor area to compensate for basal ganglia dysfunction.
authors.affiliation: University Hospital of Psychiatry, University of Bern, Bolligenstrasse 111, 3000 Bern 60, Switzerland. bracht@puk.unibe.ch
authors.forename: Tobias
authors.initials: T
authors.lastname: Bracht
authors.forename: Susanne
authors.initials: S
authors.lastname: Schnell
authors.forename: Andrea
authors.initials: A
authors.lastname: Federspiel
authors.forename: Nadja
authors.initials: N
authors.lastname: Razavi
authors.forename: Helge
authors.initials: H
authors.lastname: Horn
authors.forename: Werner
authors.initials: W
authors.lastname: Strik
authors.forename: Roland
authors.initials: R
authors.lastname: Wiest
authors.forename: Thomas
authors.initials: T
authors.lastname: Dierks
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Müller
authors.forename: Sebastian
authors.initials: S
authors.lastname: Walther
mesh_terms: D056044:Actigraphy / Q000295:instrumentation / Q000379:methods; D000328:Adult; D001479:Basal Ganglia / Q000503:physiopathology*; D056324:Diffusion Tensor Imaging / Q000295:instrumentation / Q000379:methods; D004525:Efferent Pathways / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018476:Hypokinesia / Q000503:physiopathology*; D008297:Male; D018670:Monitoring, Ambulatory; D009043:Motor Activity / Q000502:physiology*; D009044:Motor Cortex / Q000503:physiopathology*; D012559:Schizophrenia / Q000503:physiopathology*; D014836:Volition / Q000502:physiology