Is multiple system atrophy with cerebellar ataxia (MSA-C) like spinocerebellar ataxia and multiple system atrophy with parkinsonism (MSA-P) like Parkinson's disease? – A saccade study on pathophysiology. Issue 2 (February 2016)

• Record Type: Journal Article
• Authors: Terao, Yasuo; Fukuda, Hideki; Tokushige, Shinnichi; Inomata-Terada, Satomi; Yugeta, Akihiro; Hamada, Masashi; Ichikawa, Yaeko; Hanajima, Ritsuko; Ugawa, Yoshikazu
• Is Part Of: Clinical neurophysiology. Volume 127:Issue 2(2016:Feb.)
• Page Start: 1491
• Page End: 1502
• Publication Date: 2016-02
• Subjects: Saccade -- Cerebellum -- Basal ganglia -- Multiple system atrophy -- Parkinson's disease -- Pathophysiology; Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2015.07.035
• Languages: English
• ISSNs: 1388-2457

Abstract

Highlights: The pathophysiology of multiple system atrophy (MSA) was studied by saccades. Both cerebellar MSA-C and parkinsonian MSA-P subtypes show cerebellar pathophysiology in oculomotor control. In MSA-P, the direct pathway function is preserved relative to Parkinson's disease. Abstract: Objective: Patients with multiple system atrophy (MSA) are classified into those mainly manifesting cerebellar ataxia (MSA-C) and those mainly manifesting parkinsonism (MSA-P). Pathophysiological bases of these subtypes remain unclear. We hypothesized that MSA-C patients would resemble spinocerebellar degeneration patients and MSA-P patients would resemble Parkinson's disease (PD) patients in saccade abnormalities. Methods: We recorded visually guided and memory guided saccades (MGS) in 27 MSA-C and 15 MSA-P patients, as well as 50 age-matched normal subjects, 14 spinocerebellar degeneration patients showing pure cerebellar symptoms (SCD) and 61 Parkinson's disease (PD) patients. Results: Saccade parameters of both tasks showed similar changes with progressing disease in SCD and MSA-C patients, as did those of MSA-C and MSA-P patients, although hypometria was slightly more pronounced in MSA-P. In both subtypes of MSA, latency and success rate of MGS were stable throughout disease stages, whereas they deteriorated progressively with progressing disease in PD. Conclusions: Pathophysiology underlying MSA-C and MSA-P is similar as viewed from saccade performance. The MGS performance in MSA was preserved. However, MSA-P patients showed more marked hypometria, suggesting a mixture of basal ganglia pathophysiology. Significance: The similarity of saccade performance between MSA-C and MSA-P may reflect common olivopontocerebellar pathology, while the direct pathway of the basal ganglia is relatively spared compared with PD, even in MSA-P.