INTRODUCTION
Multiple system atrophy (MSA) is characterized by a combination of parkinsonism, cerebellar ataxia, autonomic dysfunction and corticospinal tract impairment [1]. There are two subtypes of MSA according to the dominant clinical features; MSA-P presenting parkinsonism and MSA-C presenting cerebellar symptoms. The cardinal features of MSA-C are common to hereditary spinocerebellar ataxia (SCA), which demonstrates variable onset ages and a slower progression. Indeed, considerable proportions of patients initially diagnosed as SCA later turned out to be MSA-C [2]. Because the initial symptoms and signs of both conditions resembles, biomarkers useful for differentiating these two diseases have been explored for many years. However, there
Multiple system atrophy (MSA) is characterized by a combination of parkinsonism, cerebellar ataxia, autonomic dysfunction and corticospinal tract impairment [1]. There are two subtypes of MSA according to the dominant clinical features; MSA-P presenting parkinsonism and MSA-C presenting cerebellar symptoms. The cardinal features of MSA-C are common to hereditary spinocerebellar ataxia (SCA), which demonstrates variable onset ages and a slower progression. Indeed, considerable proportions of patients initially diagnosed as SCA later turned out to be MSA-C [2]. Because the initial symptoms and signs of both conditions resembles, biomarkers useful for differentiating these two diseases have been explored for many years. However, there