Literature DB >> 21437717

Altered functional organization of the motor system related to ankle movements in Parkinson's disease: insights from functional MRI.

Petra Katschnig1, Petra Schwingenschuh, Margit Jehna, Martin Svehlík, Katja Petrovic, Stefan Ropele, Ernst B Zwick, Erwin Ott, Franz Fazekas, Reinhold Schmidt, Christian Enzinger.   

Abstract

Bradykinesia represents one of the cardinal and most incapacitating features of Parkinson's disease (PD). In this context, investigating the cerebral control mechanisms for limb movements and defining the associated functional neuroanatomy is important for understanding the impaired motor activity in PD. So far, most studies have focused on motor control of upper limb movements in PD. Ankle movement functional MRI (fMRI) paradigms have been used to non-invasively investigate supraspinal control mechanisms relevant for lower limb movements in healthy subjects, patients with Multiple sclerosis, and stroke. Using such an active and passive paradigm in 20 PD patients off medication (mean age 66.8 ± 7.2 years) and 20 healthy controls (HC; mean age 62.3 ± 6.9 years), we here wished to probe for possible activation differences between PD and HC and define functional correlates of lower limb function in PD. Active ankle movement versus rest was associated with a robust activation pattern in expected somatotopy involving key motor areas both in PD and HC. However, contrasting activation patterns in patients versus controls revealed excess activation in the patients in frontal regions comprising pre-supplementary motor areas (pre-SMA) and SMA proper. The extent of SMA activation did not correlate with behavioural parameters related to gait or motor function, and no differences were seen with the passive paradigm. This finding might be indicative of higher demand and increased effort in PD patients to ensure adequate motor function despite existing deficits. The missing correlation with behavioural variables and lack of differences with the passive paradigm suggests that this excess activation is not exclusively compensatory and also not hard-wired.

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Year:  2011        PMID: 21437717     DOI: 10.1007/s00702-011-0621-x

Source DB:  PubMed          Journal:  J Neural Transm (Vienna)        ISSN: 0300-9564            Impact factor:   3.575


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