title: A central processing sensory deficit with Parkinson's disease.
abstract: Parkinson's disease (PD) is a progressive degenerative disease manifested by tremor, rigidity, bradykinesia, and postural instability. Deficits in proprioceptive integration are prevalent in individuals with PD, even at early stages of the disease. These deficits have been demonstrated primarily during investigations of reaching. Here, we investigated how PD affects sensory fusion of multiple modalities during upright standing. We simultaneously perturbed upright stance with visual, vestibular, and proprioceptive stimulation, to understand how these modalities are reweighted so that overall feedback remains suited to stabilizing upright stance in individuals with PD. Eight individuals with PD stood in a visual cave with a moving visual scene at 0.2 Hz while an 80-Hz vibratory stimulus was applied bilaterally to their Achilles tendons (stimulus turns on-off at 0.28 Hz) and a ±1 mA bilateral monopolar galvanic stimulus was applied at 0.36 Hz. The visual stimulus was presented at different amplitudes (0.2°, 0.8° rotation about ankle axis) to measure: the change in gain (weighting) to vision, an intramodal effect; and a simultaneous change in gain to vibration and galvanic stimulation, both intermodal effects. Trunk/leg gain relative to vision decreased when visual amplitude was increased, reflecting an intramodal visual effect. In contrast, when vibration was turned on/off, leg gain relative to vision was equivalent in individuals with PD, indicating no reweighting of visual information when proprioception was disrupted through vibration (i.e., no intermodal effect). Trunk and leg angle gain relative to GVS also showed no reweighting in individuals with PD. These results are in contrast to previous results with healthy adults, who showed clear intermodal effects in the same paradigm, suggesting that individuals with PD not only have a proprioceptive deficit during standing, but also have a cross-modal sensory fusion deficit that is crucial for upright stance control.
authors.affiliation: Department of Kinesiology, Temple University, Philadelphia, PA, 19122, USA. sungjae.hwang@temple.edu.
authors.forename: Sungjae
authors.initials: S
authors.lastname: Hwang
authors.affiliation: Department of Kinesiology, Temple University, Philadelphia, PA, 19122, USA.
authors.forename: Peter
authors.initials: P
authors.lastname: Agada
authors.affiliation: Parkinson's & Movement Disorders Center of Maryland, Elkridge, MD, 21075, USA.
authors.forename: Stephen
authors.initials: S
authors.lastname: Grill
authors.affiliation: Department of Kinesiology, University of Maryland, College Park, MD, 20742, USA.
authors.forename: Tim
authors.initials: T
authors.lastname: Kiemel
authors.affiliation: Department of Kinesiology, Temple University, Philadelphia, PA, 19122, USA.|Department of Bioengineering, Temple University, Philadelphia, PA, 19122, USA.|Department of Kinesiology, University of Maryland, College Park, MD, 20742, USA.
authors.forename: John J
authors.initials: JJ
authors.lastname: Jeka
mesh_terms: D000125:Achilles Tendon; D000368:Aged; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000150:complications / Q000503:physiopathology*; D010468:Perceptual Disorders / Q000209:etiology / Q000503:physiopathology*; D010812:Physical Stimulation; D004856:Postural Balance / Q000502:physiology*; D011434:Proprioception / Q000502:physiology*; D014732:Vibration; D014796:Visual Perception / Q000502:physiology*
keywords: Basal ganglia; Cross-modal fusion; Parkinson’s disease; Postural instability; Sensory deficit; Sensory reweighting