Browsing by Author "Petersen, Isaac T."

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    Heterotypic Continuity of Inhibitory Control in Early Childhood: Evidence from Four Widely Used Measures
    (American Psychological Association, 2021) Petersen, Isaac T.; Bates, John E.; McQuillan, Maureen E.; Hoyniak, Caroline P.; Staples, Angela D.; Rudasill, Kathleen M.; Molfese, Dennis L.; Molfese, Victoria J.; Pediatrics, School of Medicine
    Inhibitory control has been widely studied in association with social and academic adjustment. However, prior studies have generally overlooked the potential heterotypic continuity of inhibitory control and how this could affect assessment and understanding of its development. In the present study, we systematically considered heterotypic continuity in four well-established measures of inhibitory control, testing two competing hypotheses: (1) the manifestation of inhibitory control coheres within and across time in consistent, relatively simple ways, consistent with homotypic continuity. Alternatively, (2) with developmental growth, inhibitory control manifests in more complex ways with changes across development, consistent with heterotypic continuity. We also explored differences in inhibitory control as a function of the child’s sex, language ability, and the family’s socioeconomic status. Children (N = 513) were studied longitudinally at 30, 36, and 42 months of age. Changes in the patterns of associations within and among inhibitory control measures across ages suggests that the measures’ meanings change with age, the construct manifests differently across development, and therefore, that the construct shows heterotypic continuity. We argue that the heterotypic continuity of inhibitory control motivates the use of different combinations of inhibitory control indexes at different points in development in future research to improve validity. Confirmatory factors and growth curves also suggest that individual differences in inhibitory control endure, with convergence among inhibitory control measures by 36 months of age.
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    Impaired Cerebellar-Dependent Eyeblink Conditioning in First-Degree Relatives of Individuals With Schizophrenia
    (Oxford University Press, 2014-09) Bolbecker, Amanda R.; Kent, Jerillyn S.; Petersen, Isaac T.; Klaunig, Mallory J.; Forsyth, Jennifer K.; Howell, Josselyn M.; Westfall, Daniel R.; O’Donnell, Brian F.; Hetrick, William P.; Department of Psychiatry, IU School of Medicine
    Consistent with reports of cerebellar structural, functional, and neurochemical anomalies in schizophrenia, robust cerebellar-dependent delay eyeblink conditioning (dEBC) deficits have been observed in the disorder. Impaired dEBC is also present in schizotypal personality disorder, an intermediate phenotype of schizophrenia. The present work sought to determine whether dEBC deficits exist in nonpsychotic first-degree relatives of individuals with schizophrenia. A single-cue tone dEBC paradigm consisting of 10 blocks with 10 trials each (9 paired and 1 unpaired trials) was used to examine the functional integrity of cerebellar circuitry in schizophrenia participants, individuals with a first-degree relative diagnosed with schizophrenia, and healthy controls with no first-degree relatives diagnosed with schizophrenia. The conditioned stimulus (a 400ms tone) coterminated with the unconditioned stimulus (a 50ms air puff to the left eye) on paired trials. One relative and 2 healthy controls were removed from further analysis due to declining conditioned response rates, leaving 18 schizophrenia participants, 17 first-degree relatives, and 16 healthy controls. Electromyographic data were subsequently analyzed using growth curve models in hierarchical linear regression. Acquisition of dEBC conditioned responses was significantly impaired in schizophrenia and first-degree relative groups compared with controls. This finding that cerebellar-mediated associative learning deficits are present in first-degree relatives of individuals with schizophrenia provides evidence that dEBC abnormalities in schizophrenia may not be due to medication or course of illness effects. Instead, the present results are consistent with models of schizophrenia positing cerebellar-cortical circuit abnormalities and suggest that cerebellar abnormalities represent a risk marker for the disorder.