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Antisaccade tasks can be used to index cognitive control processes, e.g. attention, behavioral inhibition, working memory, and goal maintenance in people with brain disorders. Though diagnoses of schizophrenia (SZ), schizoaffective (SAD), and bipolar I with psychosis (BDP) are typically considered to be distinct entities, previous work shows patterns of cognitive deficits differing in degree, rather than in kind, across these syndromes.
Large samples of individuals with psychotic disorders were recruited through the Bipolar-Schizophrenia Network on Intermediate Phenotypes 2 (B-SNIP2) study. Anti- and pro-saccade task performances were evaluated in 189 people with SZ, 185 people with SAD, 96 people with BDP, and 279 healthy comparison participants. Logistic functions were fitted to each group's antisaccade speed-performance tradeoff patterns.
Psychosis groups had higher antisaccade error rates than the healthy group, with SZ and SAD participants committing 2 times as many errors, and BDP participants committing 1.5 times as many errors. Latencies on correctly performed antisaccade trials in SZ and SAD were longer than in healthy participants, although error trial latencies were preserved. Parameters of speed-performance tradeoff functions indicated that compared to the healthy group, SZ and SAD groups had optimal performance characterized by more errors, as well as less benefit from prolonged response latencies. Prosaccade metrics did not differ between groups.
With basic prosaccade mechanisms intact, the higher speed-performance tradeoff cost for antisaccade performance in psychosis cases indicates a deficit that is specific to the higher-order cognitive aspects of saccade generation.
Schizotypal personality disorder (SPD) is theoretically
part of the schizophrenia spectrum both clinically and
neurobiologically. A liability for developing schizophrenia
may be associated with dysfunction of dorsolateral prefrontal
cortex (DLPFC) and its cortical and/or subcortical circuitry.
If so, abnormalities on tasks associated with DLPFC functioning
among SPD subjects would support the thesis that SPD is
neurobiologically related to schizophrenia. Antisaccade
and ocular motor delayed response performance, both of
which are ostensibly supported by DLPFC circuitry, were
assessed among 29 SPD, 17 schizophrenia, and 25 normal
subjects. Generally, the SPD subjects' performance
was more similar to normal than to schizophrenia groups.
There was evidence, however, for inhibition abnormalities
in a subgroup of SPD subjects. Antisaccade performance
identified more SPD subjects as “abnormal”
than delayed response measures.
Schizophrenia patients and their relatives have
saccadic abnormalities characterized by problems inhibiting
a response. The dorsolateral prefrontal cortex and its
associated circuitry ostensibly mediate inhibition and
support correct delayed response performance. In this context,
two components of delayed response task performance are
of interest: memory saccade metrics and error saccades
made during the delay. To evaluate these variables, an
ocular motor delayed response task was presented to 23
schizophrenia patients, 25 of their first-degree biological
relatives, and 19 normal subjects. The measure that best
differentiated groups was an increased frequency of error
saccades generated during the delay by schizophrenia subjects
and relatives. Decreased memory saccade gain also characterized
patients and relatives. The similar pattern of results
demonstrated by the patients with schizophrenia and their
relatives suggests that performance on ocular motor delayed
response tasks, either alone or in combination with other
saccadic variables, may provide useful information about
neural substrates associated with a liability for developing
The ability to identify unaffected gene carriers
within families may be crucial to the success of schizophrenia
genetics studies. Data collected from three family samples
(N = 365) demonstrated that poor antisaccade performance
is an exceptionally promising indicator of liability for
schizophrenia. A particular antisaccade task version provides
large separations (5–6 sigma) between proband and
normal groups. Poor antisaccade performance alone correctly
identified 70% of patients in California, Utah, and Micronesia
schizophrenia samples. Twenty-five to 50% of these patients'
nonpsychotic first-degree relatives also had poor antisaccade
performance, yielding risk ratios around 20:1 for simplex
and 50:1 for multiplex schizophrenia families. Poor antisaccade
performance is associated with dorsolateral prefrontal
cortex pathology, suggesting that dysfunction of this circuitry
also may predispose individuals to developing this disease.
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