Abstract
In the last few years, a lot of publications suggested that disabling cerebellar ataxias may develop through immune-mediated mechanisms. In this consensus paper, we discuss the clinical features of the main described immune-mediated cerebellar ataxias and address their presumed pathogenesis. Immune-mediated cerebellar ataxias include cerebellar ataxia associated with anti-GAD antibodies, the cerebellar type of Hashimoto’s encephalopathy, primary autoimmune cerebellar ataxia, gluten ataxia, Miller Fisher syndrome, ataxia associated with systemic lupus erythematosus, and paraneoplastic cerebellar degeneration. Humoral mechanisms, cell-mediated immunity, inflammation, and vascular injuries contribute to the cerebellar deficits in immune-mediated cerebellar ataxias.
Highlights
In the last few years, a lot of publications suggested that disabling cerebellar ataxias may develop through immune-mediated mechanisms
cerebellar ataxias (CAs) rarely occur in isolation during the first attack, they are common in established multiple sclerosis (MS) [2]
In MS, immune-mediated demyelination can occur in any area of the central nervous system (CNS) white matter and, in addition to ataxia there is a wide spectrum of neurological symptoms
Summary
In the last few years, a lot of publications suggested that disabling cerebellar ataxias may develop through immune-mediated mechanisms. Historical Scope More and more evidence suggest that cerebellar ataxias (CAs) in some patients develop through immune-mediated mechanisms.
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