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There is growing evidence that many offspring of parents with bipolar disorder (BD) will develop moderate to severe forms of psychopathology during childhood and adolescence, including thought problems. The purpose of this study was to evaluate the developmental progression of thought problems within the context of a family risk study. Repeated assessments of thought problems, spanning approximately 15 years, were conducted in offspring (N = 192 from 98 families) of parents diagnosed with BD (O-BD), unipolar depression (O-UNI), or no significant psychiatric or medical problems (O-WELL). Survival analysis showed that the O-BD group had the greatest estimated probability of developing thought problems over time, followed by O-UNI, and then O-WELL and O-BD exhibiting higher levels of persistence than O-WELL. Parent-reported thought problems in childhood and adolescence predicted a range of problems in young adulthood. Disturbances in reality testing and other atypical behaviors are likely to disrupt progression through important developmental periods and to associate with poor outcomes. These findings are likely relevant to preventing the occurrence or progression of problems in offspring of bipolar parents. The study of thought problems across development represents an important area of continued research in children at risk for development of affective disorders.
There is growing evidence that many offspring of bipolar parents will develop moderate to severe forms of psychopathology during childhood and adolescence. The purpose of this study was to apply growth curve models to evaluate developmental progression with regard to continuity and cascades representative within the context of a family risk study of bipolar disorder (BD). Repeated assessments of externalizing, internalizing, and thought problems, spanning more than a decade, were examined in a total of 94 offspring of parents with BD (O-BD), major depressive disorder (O-UNI), or no significant psychiatric or medical problems (O-WELL). Continuity was defined by the growth curve of the O-WELL group who exhibited low levels of problems from early childhood through late adolescence. Discontinuity, as evidenced by greater complexity of growth curves relative to the O-WELL group, was exhibited in the at- risk offspring groups for internalizing problems. Different patterns of developmental cascades were supported for the at-risk group with O-UNI showing a robust cascade from self-regulatory deficits (externalizing problems) to internalizing problems. There was also support for a cascade from self-regulatory deficits to thought problems across the entire group (with some support that this pattern was accounted for primarily by O-BD). This study not only serves to advance our understanding of the risks associated with a family history of BD, but also provides a novel approach to examining developmental cascades.
The findings of clinical and experimental studies conducted over the past 25 years provide extensive evidence that in both laboratory animals and man memory can be modified by treatments which affect the central nervous system. Patients with head injuries may suffer from retrograde amnesia, a loss of memory for experiences which occur just prior to the onset of the injury. Findings of laboratory studies using animal subjects indicate that retrograde amnesia can be produced by a wide variety of experimental treatments.
In a previous paper, the authors found that impairment on the
Wisconsin Card Sorting Test (WCST) in adolescence was predictive of
bipolar disorder in young adulthood among offspring of mothers with
bipolar illness. In the present study, the authors explore the
contribution of maternal characteristics, beyond maternal mood disorder,
to the prediction of offspring dysfunction on the WCST. Results showed
that maternal bipolar disorder and maternal negativity were both
predictive of impaired performance on the WCST during adolescence. The
contribution of maternal negativity to offspring WCST impairment was not
better explained by maternal personality disorder, mother's
functional impairment, family loading for bipolar disorder, or offspring
disruptive behavioral disturbance. Findings did not support a moderator
model. However, support was found for a mediation model in which maternal
negativity contributed to risk for offspring bipolar disorder through its
negative association with apparent frontal lobe functioning, as measured
by the WCST. Findings are discussed from the perspective of a
vulnerability–stress model. In addition, the authors consider the
possibility that maternal negativity and offspring impairment on the WCST
may be reflective of a common heritable trait.The findings presented in this paper come from the doctoral
dissertation of the first author, which was funded by an NIMH Intramural
Research Training Award. The authors are enormously grateful to Anne
Mayfield, without whom this project would not have been possible. We are
deeply indebted to Ann S. Masten, W. Andrew Collins, L. Alan Sroufe,
Monica Luciana, and Carrie Borchardt, who provided support and guidance
throughout all stages of this project. We are also thankful to Robert
Asarnow for his advice and encouragement, and to Roger E. Meyer and Daniel
N. Klein for their comments on earlier drafts of this paper. In addition,
we acknowledge the contributions of Gail Inoff-Germain, who administered
diagnostic interviews and neuropsychological measures at adolescent
follow-up; Rula B. Garside, who undertook the painstaking job of
establishing interrater reliability; Erika Sundstrom, who devoted many
hours to data organization and quality assurance; and Sara Avery Torvik
and Patricia Kasdan, whose combined gifts of organization and warmth
created a comfortable atmosphere for study participants. Finally, we thank
the extraordinary research participants of the NIMH Childrearing Study,
who have shown enormous bravery and dedication by sharing with us 23 years
of their lives.
Studies of adults who have been diagnosed with, and treated for,
bipolar disorder have shown that these patients exhibit impairment on
measures of executive functioning. However, it is unclear whether
executive dysfunction precedes the diagnosis of bipolar illness, or
develops subsequent to its onset. Moreover, investigators have failed
to control for the effects of premorbid attentional problems on
cognitive performance in these patients. The present authors explored
these questions using data from a longitudinal prospective study of
individuals at risk for major mood disorder. Results revealed that 67%
of participants who met criteria for bipolar disorder in young
adulthood showed impairment on the Wisconsin Card Sorting Test (WCST)
when they were assessed during adolescence, as compared with 17% of
individuals with no major mood diagnosis, and 19% with unipolar
depression. This association between performance on the WCST and
bipolar illness was not accounted for by high rates of premorbid
attentional disturbance. In fact, among participants with early
attentional problems, only those who ultimately developed bipolar
disorder exhibited impairment on the WCST. Early attentional problems
that preceded unipolar depression or no mood disorder were not
associated with executive dysfunction.The findings presented in this paper come from the doctoral
dissertation of the first author, which was funded by an NIMH
Intramural Research Training Award. The authors are enormously grateful
to Roger E. Meyer for his comments on earlier drafts of this paper and
to Anne Mayfield, without whom this project would not have been
possible. We are deeply indebted to Ann S. Masten, W. Andrew Collins,
L. Alan Sroufe, Monica Luciana, and Carrie Borchardt, who provided
invaluable guidance throughout all stages of this project, as well as
Robert Asarnow, who was an important mentor during the review process.
In addition, we acknowledge the contributions of Gail
Inoff–Germain, who administered diagnostic interviews and
neuropsychological measures at adolescent follow-up; Rula B. Garside,
who undertook the painstaking job of establishing interrater
reliability; Erika Sundstrom, who devoted many hours to data
organization and quality assurance; and Sara Avery Torvik and Patricia
Kasdan, whose combined gifts of organization and warmth created a
comfortable atmosphere for study participants. Finally, we thank the
extraordinary research participants of the NIMH Childrearing Study, who
have shown enormous bravery and dedication by sharing with us 23 years
of their lives.
From a transactional developmental perspective, the authors review findings from studies of
animals and humans regarding a proposed relation between stress system abnormalities and major
depression. The stress system has evolved to promote successful adaptation across the life span,
but disruptions in its functioning may increase the risk of pathological outcomes. Emphasis is
placed on the role of prenatal and early postnatal experience in contributing to individual
differences in postnatal stress reactivity, which may interact with cognitive and psychosocial
vulnerabilities to increase susceptibility to later onset of depression. Findings regarding cognitive,
psychosocial, and medical sequelae of depression are also reviewed, with a focus on the possible
mediating role of the stress system. The authors highlight the importance of multidisciplinary,
longitudinal studies in attempting to gain a deeper understanding of the complex developmental
processes involved in the onset and course of depression.
Levels of vasopressin, somatostatin, neurotensin, vasoactive intestinal peptide, corticotrophin-releasing factor and adrenocorticotrophin in CSF were determined in lithium-treated and unmedicated euthymic bipolar patients and controls, in a search for a trait marker in affective disorder. No group differences in levels of these peptides were found. Highly significant positive correlations were found among these peptides (with the exception of neurotensin), suggesting that their presence in CSF is functionally significant, as opposed to the result of random diffusion from the interstitial space of the brain.
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