The role of the frontal eye fields in the oculomotor inhibition of reflexive saccades: Evidence from lesion patients

Executive deficit in spinocerebellar ataxia type 2 is related to expanded CAG repeats: Evidence from antisaccadic eye movements

“…Therefore, the neurodegenerative changes documented for caudate nucleus and substantia nigra in SCA2 patients (Estrada et al, 1999) could also explain the significant failure to inhibit the automatic visually guided pro-saccades in these subjects. Also, the putative involvement of frontal eye field may contribute to antisaccade impairments since this region is involved in the generation of central commands for intentional correct antisaccades (Brown, Vilis, & Everling, 2007;Van der Stigchel, van Koningsbruggen, Nijboer, List, & Rafal, 2012).…”

Antisaccade performance in Korsakoff patients reveals deficits in oculomotor inhibition

“…As mentioned in the introduction, an elevated number of antisaccade errors have been linked to deficits in frontal areas (Guitton et al, 1985;Pierrot-Deseilligny et al, 2003;Pierrot-Deseilligny et al, 1991;Van der Stigchel et al, 2012). Various frontal areas, like the dorsolateral prefrontal cortex and the frontal eye fields, project to the superior colliculus, a motor map in the midbrain in which the competition between possible saccade goals is assumed to be resolved (Munoz, 2002).…”

“…Trials in which no saccades were made or in which all saccades were too small (<2 • ) were excluded as well. These inclusion criteria are similar to those applied in studies on antisaccade performance in frontal lesion patients (e.g., Van der Stigchel et al, 2012).…”

“…Therefore, the chosen inclusion criteria with respect to start and endpoint of the saccade had to be more liberal than in, for instance, antisaccade studies in frontal lesion patients in order to include enough trials for a solid analysis (e.g., Van der Stigchel et al, 2012). For both anti-and prosaccades, the first saccade after the presentation of the onset needed to be initiated from a distance of 5.25 • from the centre of the display (half the distance between the centre of the display and the onset location), irrespective of the location of the onset in the display.…”

“…For instance, imaging studies have identified several frontal areas that are active during the antisaccade task such as the frontal eye fields, supplementary eye fields, and dorsolateral prefrontal cortex (Funahashi, Bruce, & Goldman-Rakic, 1993;Munoz & Everling, 2004). Lesion studies have revealed that successful inhibition in the antisaccade task relies heavily on frontal circuits, as patients with frontal lesions execute more erroneous eye movements towards a contralesional stimulus onset (Guitton, Buchtel, & Douglas, 1985;Pierrot-Deseilligny et al, 2003;Pierrot-Deseilligny, Rivaud, Gaymard, & Agid, 1991;Van der Stigchel, van Koningsbruggen, Nijboer, List, & Rafal, 2012). An elevated amount of directional eye movement errors in the antisaccade task is therefore generally linked to deficits associated with the frontal cortex (Everling & Munoz, 2000;Funahashi et al, 1993).…”