Motion integration deficits are independent of magnocellular impairment in Parkinson's disease

• Type: Article in International Scientific Journal
• Date: 2009

Authors

Miguel Castelo-Branco (Author) Other; Mafalda Mendes (Author) Other; Fátima Silva (Author) Other; João Massano (Author) FMUP; Gustavo Januário (Author) Other; Cristina Januário (Author) Other; António Freire (Author) Other

Journal

Title: Neuropsychologia

Vol. 47

Pages: 314-320

ISSN: 0028-3932

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 26 Citations

Scopus - 28 Citations

Pubmed / Medline

Scientific classification

CORDIS: Health sciences > Neuroscience > Neurology

Other information

Authenticus ID: P-003-RF0

DOI: 10.1016/j.neuropsychologia.2008.09.003

Abstract (EN): Motion processing involves multiple hierarchical steps, from the magnocellular pathway, sensitive to high temporal frequency modulations, to subsequent motion integration within the visual cortical dorsal stream. We have tested whether motion integration deficits in mild Parkinson disease (PD) can be explained by visual deficits in earlier processing nodes. Contrast sensitivity deficits in the magnocellular pathway. were compared with speed discrimination of local dots moving in random directions, speed and direction discrimination of moving surfaces and motion integration as measured by 2D coherence thresholds (n = 27). We have found that low-level magnocellular impairment in PD does not explain deficits in subsequent steps in motion processing. High-level performance was abnormal in particular for tasks requiring perception of coherently moving surfaces. Motion coherence deficits were predictive of visuomotor impairment. corroborating a previous magnetic stimulation study in normal subjects. We conclude that dorsal stream deficits in PD have a high-level visual cortical basis independent of low-level magnocellular damage.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 7