title: Saccade abnormalities associated with focal cerebral lesions - How cortical and basal ganglia commands shape saccades in humans.
abstract: To study saccade abnormalities associated with focal cerebral lesions, including the cerebral cortex and basal ganglia (BG).
  
  
  
  We studied the latency and amplitude of reflexive and voluntary saccades in 37 patients with focal lesions of the frontal and parietal cortices and BG (caudate and putamen), and 51 age-matched controls, along with the ability to inhibit unwanted reflexive saccades.
  
  
  
  Latencies of reflexive saccades were prolonged in patients with parietal lesions involving the parietal eye field (PEF), whereas their amplitude was decreased with parietal or putaminal lesions. In contrast, latency of voluntary saccades was prolonged and their success rate reduced with frontal lesions including the frontal eye field (FEF) or its outflow tract as well as the dorsolateral/medial prefrontal cortex, and caudate lesions, whereas their amplitude was decreased with parietal lesions. Inhibitory control of reflexive saccades was impaired with frontal, caudate and, less prominently, parietal lesions.
  
  
  
  PEF is important in triggering reflexive saccades, also determining their amplitude. Whereas FEF and the caudate emit commands for initiating voluntary saccades, their amplitude is mainly determined by PEF. Commands not only from FEF and dorsolateral/medial prefrontal cortex but also from the caudate and PEF serve to inhibit unnecessary reflexive saccades.
  
  
  
  The findings suggested how cortical and BG commands shape reflexive and voluntary saccades in humans.
authors.affiliation: Department of Neurology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. Electronic address: yterao-tky@umin.ac.jp.
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Terao
authors.affiliation: Segawa Neurological Clinic for Children, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Fukuda
authors.affiliation: Department of Neurology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
authors.forename: Shinnichi
authors.initials: S
authors.lastname: Tokushuge
authors.affiliation: Segawa Neurological Clinic for Children, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Nomura
authors.affiliation: Department of Neurology, School of Medicine, Kitasato University, Japan.
authors.forename: Ritsuko
authors.initials: R
authors.lastname: Hanajima
authors.affiliation: Department of Neurology, School of Medicine, Fukushima Medical University, Japan.
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Ugawa
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D001479:Basal Ganglia / Q000503:physiopathology*; D020520:Brain Infarction / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000503:physiopathology*; D004569:Electroencephalography; D005260:Female; D006801:Humans; D020300:Intracranial Hemorrhages / Q000503:physiopathology*; D008875:Middle Aged; D012438:Saccades / Q000502:physiology*
keywords: Amplitude; Basal ganglia; Cerebral cortex; Inhibition; Latency; Saccade