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

• Published in: Journal of the neurological sciences Vol. 306; no. 1; pp. 103 - 107
• Main Authors: Rodríguez-Labrada, Roberto, Velázquez-Pérez, Luis, Seigfried, Carola, Canales-Ochoa, Nalia, Auburger, Georg, Medrano-Montero, Jacqueline, Sánchez-Cruz, Gilberto, Aguilera-Rodríguez, Raúl, Laffita-Mesa, José, Vázquez-Mojena, Yaimeé, Verdecia-Ramirez, Marisleydis, Motta, Maribel, Quevedo-Batista, Yudith
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 15-07-2011; Elsevier
• Subjects: Analysis of Variance; Ataxins; Biological and medical sciences; Biomarker; Cognition Disorders - etiology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Executive Function - physiology; Female; Frontal Lobe - physiopathology; Frontal-executive functions; Genetic Testing; Humans; Linear Models; Male; Medical sciences; Nerve Tissue Proteins - genetics; Neurologic Examination; Neurology; Neuropsychological Tests; Ocular Motility Disorders - etiology; Reaction Time - physiology; Saccades - physiology; Saccadic latency; Saccadic movements; SCA2; Spinocerebellar Ataxia; Spinocerebellar Ataxias - complications; Spinocerebellar Ataxias - genetics; Spinocerebellar Ataxias - pathology; Trinucleotide Repeat Expansion - genetics; Saccadic latency; Saccadic movements; Biomarker; Spinocerebellar Ataxia; Frontal-executive functions; SCA2; Executive function; Nervous system diseases; Cognitive disorder; Genetic disease; Spinocerebellar ataxia; Central nervous system disease; Frontal; Degenerative disease
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/j.jns.2011.03.033

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.