Saccadic disinhibition in schizophrenia patients and their first-degree biological relatives - A parametric study of the effects of increasing inhibitory load

Citation
Ce. Curtis et al., Saccadic disinhibition in schizophrenia patients and their first-degree biological relatives - A parametric study of the effects of increasing inhibitory load, EXP BRAIN R, 137(2), 2001, pp. 228-236
Citations number
54
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL BRAIN RESEARCH
ISSN journal
00144819 → ACNP
Volume
137
Issue
2
Year of publication
2001
Pages
228 - 236
Database
ISI
SICI code
0014-4819(200103)137:2<228:SDISPA>2.0.ZU;2-V
Abstract
Several studies have reported that patients with schizophrenia and their re latives perform poorly on antisaccade tasks and have suggested that this de ficit represents saccadic disinhibition. If this proposition is correct, th en varying task parameters that specifically increase the difficulty with w hich unwanted saccades can be inhibited should exacerbate deficits. Forty-t wo schizophrenia patients, 42 of their first-degree biological relatives, 2 1 psychotic affective disorder patients, and 38 nonpsychiatric comparison s ubjects were given fixation and antisaccade tasks. The introduction of dist racters and the presence of visible fixation stimuli were parameters used t o vary the difficulty in suppressing unwanted saccades (inhibitory load). I t is known that the presence of a fixation stimulus at the time when a sacc ade must be inhibited results in fewer reflexive errors on antisaccade task s. Performance on fixation tasks without (low load) vs with distracters (hi gh load) and antisaccade tasks that had fixation stimuli still visible (low load) vs already extinguished (high load) at the time when the reflexive s accade must be inhibited was compared. The schizophrenia patients and their first-degree biological relatives showed evidence of increased saccadic di sinhibition that was most pronounced during high inhibitory load conditions . These data indicate that dysfunctional inhibitory processes, at least in the oculomotor domain, are associated with the liability to schizophrenia. Results also suggest that this genetic liability may be related to dysfunct ional prefrontal cortical areas that provide top-down inhibitory control ov er reflexive saccade generation.