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Articles by A Polcari
Total Records ( 2 ) for A Polcari
  M. H Teicher , J. A Samson , Y. S Sheu , A Polcari and C. E. McGreenery
  Objective:

Previous studies have shown that exposure to parental verbal abuse in childhood is associated with higher rates of adult psychopathology and alterations in brain structure. In this study the authors sought to examine the symptomatic and neuroanatomic effects, in young adulthood, of exposure to peer verbal abuse during childhood.

Method:

A total of 848 young adults (ages 18–25 years) with no history of exposure to domestic violence, sexual abuse, or parental physical abuse rated their childhood exposure to parental and peer verbal abuse and completed a self-report packet that included the Kellner Symptom Questionnaire, the Limbic Symptom Checklist–33, and the Dissociative Experiences Scale. Diffusion tensor images were collected for a subset of 63 young adults with no history of abuse or exposure to parental verbal abuse selected for varying degrees of exposure to peer verbal abuse. Images were analyzed using tract-based spatial statistics.

Results:

Analysis of covariance revealed dose-dependent effects of peer verbal abuse on anxiety, depression, anger-hostility, dissociation, "limbic irritability," and drug use. Peer and parental verbal abuse were essentially equivalent in effect size on these ratings. Path analysis indicated that peer verbal abuse during the middle school years had the most significant effect on symptom scores. Degree of exposure to peer verbal abuse correlated with increased mean and radial diffusivity and decreased fractional anisotropy in the corpus callosum and the corona radiata.

Conclusions:

These findings parallel results of previous reports of psychopathology associated with childhood exposure to parental verbal abuse and support the hypothesis that exposure to peer verbal abuse is an aversive stimulus associated with greater symptom ratings and meaningful alterations in brain structure.

  K Ohashi , G Vitaliano , A Polcari and M. H. Teicher
 

Context  Seated hyperactivity is a defining feature of the combined and predominantly hyperactive-impulsive subtypes of attention-deficit/hyperactivity disorder (ADHD), but its underlying nature is unknown.

Objective  To determine whether hyperactivity is a consequence of an impaired ability to inhibit activity to low levels or to maintain positional stability.

Design  Case-control study.

Setting  Academic research center and school.

Participants  Sixty-two boys 9 to 12 years of age (of 73 screened), recruited from the community by advertisement, who met DSM-IV criteria for ADHD combined subtype on structured interview. Sixty-two controls were selected by matching for age and sex from a community sample of 1168 subjects in 3 participating school districts. Pupils with Conners' Teacher Rating Scores Revised within ±1 SD of the mean for age were eligible for randomized matching.

Intervention  Infrared motion analysis of head-marker movements (50 Hz) during performance of a 15-minute cognitive control task. Subjects with ADHD were tested at least 18 hours following their last dose of methylphenidate and again 120 minutes after a 0.4-mg/kg probe dose.

Main Outcome Measures  Inhibitory control (spike and basal amplitude) and head-marker stability (approximate entropy, Lyapunov, and spectral exponents).

Results  Inhibitory control measures were 2-fold higher in subjects with ADHD (d' = 0.63-0.95). Group differences in head-marker stability were even greater (d' = 2.20-4.71; receiver operating characteristic area = 0.956-1.0). Methylphenidate restored inhibitory ability to control levels but only partially corrected stability deficits, which still distinguished subjects with ADHD from controls (receiver operating characteristic area = 0.722-0.995).

Conclusions  Children with ADHD have a deficient ability to inhibit activity to low levels and unstable control of head-marker position characterized by deterministic chaos (sensitivity to initial conditions). These deficits differed in degree of correctability by methylphenidate, suggesting that they may be mediated by different neural circuits (eg, corticostriatal vs cerebrovestibular).

 
 
 
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