Antisaccade performance is abnormal in schizophrenia patients but not in their biological relatives

Brownstein, Joanna; Krastoshevsky, Olga; McCollum, Courtney; Kundamal, Sapna; Matthysse, Steven; Holzman, Philip S.; Mendell, Nancy R.; Levy, Deborah L.

doi:10.1016/s0920-9964(02)00438-3

Cited by 58 publications

(54 citation statements)

References 45 publications

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“…Antagonism of serotonin 5-HT 2 receptors and, indirectly, action on prefrontal dopaminergic transmission may reduce the antisaccade error rate (38). Treatment with atypical antipsychotics may normalize antisaccade latency in previously untreated or drug-naive patients with schizophrenia; however, risperidone may prolong latency (for review, see references 39,40). Typical neuroleptic treatment does not seem to affect P50 sensory gating deficits in subjects with schizophrenia (41).…”

Section: Discussionmentioning

confidence: 99%

A Concordance Study of Three Electrophysiological Measures in Schizophrenia

Chapelle¹,

Nkam²,

Houy³

et al. 2005

AJP

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Despite superficial similarities, two paradigms designed to measure central inhibition processes (antisaccade and P50 inhibition) do not appear to reflect the same neurobiological substrates. In contrast, the convergence in performance data for the antisaccade and eye tracking paradigms suggests that the neural circuitry underlying these tasks may overlap. P50 inhibition and antisaccade errors were the optimal paradigms for discrimination between comparison subjects, patients with schizophrenia, and the parents of patients with schizophrenia.

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Section: Discussionmentioning

confidence: 99%

A Concordance Study of Three Electrophysiological Measures in Schizophrenia

Chapelle¹,

Nkam²,

Houy³

et al. 2005

AJP

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“…91,92 Two meta-analyses found evidence for impairments in nonpsychotic first-degree relatives of schizophrenia patients relative to healthy controls (mean Cohen's d = 0.43 93 and 0.61 94 ) although there are studies that have failed to find this effect. 95 Impairments in AS have also been found in clinically unaffected twins discordant for schizophrenia. 96 …”

Section: Antisaccade Taskmentioning

confidence: 99%

Electrophysiological Endophenotypes for Schizophrenia

Owens

Bachman

Glahn

et al. 2016

Harvard Review of Psychiatry

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Endophenotypes are quantitative, heritable traits that may help to elucidate the pathophysiologic mechanisms underlying complex disease syndromes, such as schizophrenia. They can be assessed at numerous levels of analysis; here, we review electrophysiological endophenotypes that have shown promise in helping us understand schizophrenia from a more mechanistic point of view. For each endophenotype, we describe typical experimental procedures, reliability, heritability, and reported gene and neurobiological associations. We discuss recent findings regarding the genetic architecture of specific electrophysiological endophenotypes, as well as converging evidence from EEG studies implicating disrupted balance of glutamatergic signaling and GABA-ergic inhibition in the pathophysiology of schizophrenia. We conclude that refining the measurement of electrophysiological endophenotypes, expanding genetic association studies, and integrating datasets are important next steps for understanding the mechanisms that connect identified genetic risk loci for schizophrenia to the disease phenotype.

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“…Functional neuroimaging has linked these deficits to decreased recruitment of the caudate, putamen, and globus pallidus (Crawford, Puri, Nijran, Jones, Kennard, & Lewis,1996;Raemaekers et al, 2002;Raemaekers, Ramsey, Vink, van den Heuvel, & Kahn, 2006). Although impairments in saccade inhibition are not specific to schizophrenia (Brownstein et al, 2003;Munoz & Everling, 2004), these data suggest that the antisaccade task may be sensitive to neural deficits implicated in the disorder (Hutton & Ettinger, 2006). Go/NoGo and Stop-signal tasks-Inhibition of manual motor responses in go/nogo and stop-signal tasks also depends upon the interaction of frontal and basal ganglia control regions with motor output structures, including the thalamus and primary motor cortex ( Figure 3; for review, see Band & van Boxtel, 1999).…”

Section: Neurobiological Mechanisms Of Response Inhibitionmentioning

confidence: 99%

Inhibition of action, thought, and emotion: A selective neurobiological review

Dillon

Pizzagalli

2007

Applied and Preventive Psychology

167

137

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The neural bases of inhibitory function are reviewed, covering data from paradigms assessing inhibition of motor responses (antisaccade, go/nogo, stop-signal), cognitive sets (e.g., Wisconsin Card Sort Test), and emotion (fear extinction). The frontal cortex supports performance on these paradigms, but the specific neural circuitry varies: response inhibition depends upon fronto-basal ganglia networks, inhibition of cognitive sets is supported by orbitofrontal cortex, and retention of fear extinction reflects ventromedial prefrontal cortexamygdala interactions. Inhibition is thus neurobiologically heterogeneous, although right ventrolateral prefrontal cortex may support a general inhibitory process. Dysfunctions in these circuits may contribute to psychopathological conditions marked by inhibitory deficits.

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Antisaccade performance is abnormal in schizophrenia patients but not in their biological relatives

Cited by 58 publications

References 45 publications

A Concordance Study of Three Electrophysiological Measures in Schizophrenia

A Concordance Study of Three Electrophysiological Measures in Schizophrenia

Electrophysiological Endophenotypes for Schizophrenia

Inhibition of action, thought, and emotion: A selective neurobiological review

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