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The Aetiologic Spectrum of Cerebellar Ataxia: Acquired Causes of Ataxia

  1. Peter K Todd1,
  2. J Paul Taylor2

Published Online: 15 MAR 2009

DOI: 10.1002/9780470015902.a0021592



How to Cite

Todd, P. K. and Taylor, J. P. 2009. The Aetiologic Spectrum of Cerebellar Ataxia: Acquired Causes of Ataxia. eLS. .

Author Information

  1. 1

    University of Michigan Medical School, Ann Arbor, Michigan, USA

  2. 2

    St. Jude Children' Research Hospitals, Memphis, Tennesee, USA

Publication History

  1. Published Online: 15 MAR 2009


Ataxia is a common finding in patients seen in neurological practice and can be the result of a wide variety of causes. Although cerebellar degeneration can be chronic and slowly progressive, acute cerebellar swelling due to infarction, oedema or haemorrhage can have rapid and catastrophic effects and is a true neurological emergency. Here we set out to briefly describe the clinical/anatomical correlates of cerebellar disease and to provide a broad differential diagnosis for patients who present with cerebellar ataxia. This article specifically focuses on acquired causes of cerebellar ataxia. A separate complementary article discusses common hereditary causes of cerebellar ataxia.

Key Concepts

  • Clinical syndromes associated with cerebellar dysfunction may be divided into syndromes that predominantly affect the midline cerebellar structures (gait and ocular dysfunction predominant) or the cerebellar hemisphere(s) (ipsilateral appendicular ataxia, dysarthria).

  • Acute onset of cerebellar ataxia is most commonly associated with vascular disorders (stroke or haemorrhage), toxins or infectious aetiologies.

  • Subacute onset cerebellar ataxia can result from a variety of causes, including infectious, neoplastic, autoimmune and metabolic abnormalities. Many of these causes of ataxia are treatable.

  • Most slowly progressive cerebellar ataxias result from neurodegenerative aetiologies, either inherited or sporadic.


  • multiple sclerosis;
  • paraneoplastic cerebellar degeneration;
  • vitamin E deficiency;
  • multiple system atrophy;
  • toxins