Childhood-Onset Bipolar Disorder

University of Pittsburgh, Pittsburgh, Pennsylvania, United States
Journal of the American Academy of Child & Adolescent Psychiatry (Impact Factor: 7.26). 03/2007; 46(2):197-204. DOI: 10.1097/01.chi.0000246069.85577.9e
Source: PubMed


To determine whether childhood-onset bipolar disorder (BP) is associated with an increased psychiatric family history compared with adolescent-onset BP.
Semistructured psychiatric interviews were conducted for 438 youth with BP spectrum disorders. To evaluate the effects of age at onset and psychiatric family history, the sample was divided into childhood-onset BP (age and BP onset <12 years; n = 192), adolescents with early-onset BP (age > or =12 years and BP onset <12 years; n = 136), and adolescents with late-onset BP (age and BP onset > or =12 years; n = 110). Lifetime family history of psychiatric illness was ascertained for first- and second-degree relatives through both direct interview of caretakers and the Family History Screen.
After significant demographic and clinical factors were controlled for, children and adolescents with childhood-onset BP showed higher percentages of positive first-degree family history for depression, anxiety, attention-deficit/hyperactivity, conduct, and substance dependence disorders and suicidal behaviors compared with adolescents with late onset. Subjects with childhood-onset BP also showed elevated familial loading for depression and attention-deficit/hyperactive disorder in second-degree relatives.
These data support a model that postulates a higher density of familial risk for a broad range of psychopathology in childhood-onset BP.

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    • "Of particular concern, the pooled approach did not detect a significant relationship between early-onset and having a first-degree relative with mood disorder. Thus, this finding would be in contradiction with several prior studies demonstrating relationships between genetic loading and childhood-onset bipolar disorder (Heleniuset al., 2013; Leboyer and Henry, 2005; Lin et al., 2006; Rende et al., 2007; Schurhoff et al., 2003), emphasizing that very early-onset patients may be driving these findings. As expected, illness duration was markedly longer for patients with childhood-(25.4 years) compared to adolescent-(16.7 years) and adultonset (13.8 years) bipolar disorder – indeed, illness duration may mediate relationships between early-onset and unfavorable illness characteristics. "
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    ABSTRACT: The strengths and limitations of considering childhood-and adolescent-onset bipolar disorder (BD) separately versus together remain to be established. We assessed this issue. BD patients referred to the Stanford Bipolar Disorder Clinic during 2000-2011 were assessed with the Systematic Treatment Enhancement Program for BD Affective Disorders Evaluation. Patients with childhood- and adolescent-onset were compared to those with adult-onset for 7 unfavorable bipolar illness characteristics with replicated associations with early-onset patients. Among 502 BD outpatients, those with childhood- (<13 years, N=110) and adolescent- (13-18 years, N=218) onset had significantly higher rates for 4/7 unfavorable illness characteristics, including lifetime comorbid anxiety disorder, at least ten lifetime mood episodes, lifetime alcohol use disorder, and prior suicide attempt, than those with adult-onset (>18 years, N=174). Childhood- but not adolescent-onset BD patients also had significantly higher rates of first-degree relative with mood disorder, lifetime substance use disorder, and rapid cycling in the prior year. Patients with pooled childhood/adolescent - compared to adult-onset had significantly higher rates for 5/7 of these unfavorable illness characteristics, while patients with childhood- compared to adolescent-onset had significantly higher rates for 4/7 of these unfavorable illness characteristics. Caucasian, insured, suburban, low substance abuse, American specialty clinic-referred sample limits generalizability. Onset age is based on retrospective recall. Childhood- compared to adolescent-onset BD was more robustly related to unfavorable bipolar illness characteristics, so pooling these groups attenuated such relationships. Further study is warranted to determine the extent to which adolescent-onset BD represents an intermediate phenotype between childhood- and adult-onset BD. Copyright © 2015 Elsevier B.V. All rights reserved.
    Full-text · Article · Mar 2015 · Journal of Affective Disorders
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    • "Rende et al (Rende et al., 2007) reported that 33% of children with BP-I disorder had a family history of ADHD and, although the morbid risk of ADHD was not specifically estimated, Geller et al (Geller et al., 2006) found that relatives with ADHD, of child bipolar probands, were at increased risk for bipolar disorder. The familial relationship between ADHD and BP-I observed in these studies of BP-I probands (Geller et al., 2006, Rende et al., 2007) is consistent with our previous family studies of ADHD and BP-I (Faraone et al., 1997, Faraone et al., 2001, Wozniak et al., 1995b). That these disorders may also share familial risk factors could explain the association of the dopamine transporter gene with both bipolar disorder (Greenwood et al., 2006, Mick et al., 2007) and ADHD (Asherson et al., 2007, Brookes et al., 2006a, Brookes et al., 2006b). "
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    ABSTRACT: To estimate the spectrum of familial risk for psychopathology in first-degree relatives of children with unabridged DSM-IV bipolar-I disorder (BP-I). We conducted a blinded, controlled family study using structured diagnostic interviews of 157 children with BP-I probands (n=487 first-degree relatives), 162 attention deficit hyperactivity disorder (ADHD) (without BP-I) probands (n=511 first-degree relatives), and 136 healthy control (without ADHD or BP-I) probands (n=411 first-degree relatives). The morbid risk (MR) of BP-I disorder in relatives of BP-I probands (MR=0.18) was increased 4-fold [95% confidence interval (CI) 2.3-6.9, p<0.001] over the risk to relatives of control probands (MR=0.05) and 3.5-fold (95% CI 2.1-5.8, p<0.001) over the risk to relatives of ADHD probands (MR=0.06). In addition, relatives of children with BP-I disorder had high rates of psychosis, major depression, multiple anxiety disorders, substance use disorders, ADHD and antisocial disorders compared with relatives of control probands. Only the effect for antisocial disorders lost significance after accounted for by the corresponding diagnosis in the proband. Familial rates of ADHD did not differ between ADHD and BP-I probands. Our results document an increased familial risk for BP-I disorder in relatives of pediatric probands with DSM-IV BP-I. Relatives of probands with BP-I were also at increased risk for other psychiatric disorders frequently associated with pediatric BP-I. These results support the validity of the diagnosis of BP-I in children as defined by DSM-IV. More work is needed to better understand the nature of the association between these disorders in probands and relatives.
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    • "The interviewer indicates whether participants endorsed the presence of these symptoms using a 3-point scale (0=not present, 1=present, and 9=don't know) and which relative was affected. We considered family members to be positive for a disorder if the interviewer coded a " 1 " for " definite " endorsement of an item consistent with other research (Rende et al., 2007). The calculation for family loading for five family history variables (PTSD, anxiety, depression, alcohol use disorders, and drug use disorders) was adapted from previous research (Johnson & Pickens, 2001; Milne et al., 2008), and determined by summing the total number of first degree full biological relatives who, based on the reports of the recruits, screened positive ( " definite " ) for symptoms, separately for each family history variable, divided by the total number of first degree relatives, providing an estimate of family loading for that variable. "
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    ABSTRACT: Family history of psychiatric and substance use disorders has been associated with posttraumatic stress disorder (PTSD) in cross-sectional studies. Using a prospective design, we examined the relationships of family history of psychiatric and substance use disorders to posttraumatic stress symptoms in 278 healthy police recruits. During academy training, recruits were interviewed on family and personal psychopathology, prior cumulative civilian trauma exposure, and completed self-report questionnaires on nonspecific symptoms of distress and alcohol use. Twelve months after commencement of active duty, participants completed questionnaires on critical incident exposure over the previous year, peritraumatic distress to the worst critical incident during this time, and posttraumatic stress symptoms. A path model indicated: (1) family loading for mood and anxiety disorders had an indirect effect on posttraumatic stress symptoms at 12 months that was mediated through peritraumatic distress to the officer's self-identified worst critical incident, (2) family loading for substance use disorders also predicted posttraumatic stress symptoms at 12 months and this relationship was mediated through peritraumatic distress. These findings support a model in which family histories of psychopathology and substance abuse are pre-existing vulnerability factors for experiencing greater peritraumatic distress to critical incident exposure which, in turn, increases the risk for development of symptoms of posttraumatic stress disorder. Replication in other first responders, military and civilians will be important to determine generalizability of these findings.
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