Saccadic latency is prolonged in Spinocerebellar Ataxia type 2 and correlates with the frontal-executive dysfunctions

J Neurol Sci. 2011 Jul 15;306(1-2):103-7. doi: 10.1016/j.jns.2011.03.033. Epub 2011 Apr 9.

Abstract

Data on saccadic latency in patients with Spinocerebellar Ataxia 2 (SCA2) are sparse and contradictory. In order to determine whether saccadic latency is definitely prolonged, identify its possible determinants and evaluate it as disease biomarker we assessed the saccadic latency by electronystagmography in 110 SCA2 patients and their paired controls. Mean saccadic latencies were significantly longer in patients when compared to controls for all tested target displacements. Forty-six percent of SCA2 patients had saccadic latencies above the normal range. Reciprobit plots of saccadic latency demonstrated a skewed distribution in the direction of longer latencies for the patients compared to controls. As saccadic latency increased, the velocity and amplitude of saccades significantly decreased in SCA2 subjects but not in controls. Saccadic latency was not influenced by any demographical, clinical or molecular SCA2 variables, but it showed a significant correlation with the performance of the Stroop test, the verbal fluency test and the Wisconsin Card Sorting Test in SCA2 patients. This paper demonstrated that saccadic latency is prolonged in SCA2 patients and it significantly correlates with the performance of frontal-executive functions, thus this parameter could be a useful biomarker to evaluate the efficiency of future therapeutical options on these dysfunctions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Ataxins
  • Cognition Disorders / etiology*
  • Executive Function / physiology*
  • Female
  • Frontal Lobe / physiopathology*
  • Genetic Testing
  • Humans
  • Linear Models
  • Male
  • Nerve Tissue Proteins / genetics
  • Neurologic Examination
  • Neuropsychological Tests
  • Ocular Motility Disorders / etiology*
  • Reaction Time / physiology
  • Saccades / physiology*
  • Spinocerebellar Ataxias / complications*
  • Spinocerebellar Ataxias / genetics
  • Spinocerebellar Ataxias / pathology
  • Trinucleotide Repeat Expansion / genetics

Substances

  • Ataxins
  • Nerve Tissue Proteins