Relatively little is known about the longitudinal course of bipolar disorder in children (1
). Some adult mood researchers (2
) hypothesize that unipolar depression and bipolar disorder [mainly bipolar II disorder (BP-II)] lie on a dimensional continuum, as they share several common features (age at onset, atypical depressive features, depressive mixed state, number of recurrences, and genetic vulnerability).
Even less is known about the full spectrum of bipolar disorder in children [bipolar spectrum disorders (BPSD): bipolar I disorder (BP-I), BP-II, cyclothymia, and bipolar disorder not otherwise specified (BP-NOS)]. Only one longitudinal study, the Course and Outcome of Bipolar Youth (COBY)
has examined manic symptoms in children diagnosed with BPSD (4
). No studies to date have longitudinally assessed the clinical importance of transient manic symptoms (TMS) in children with depressive spectrum disorders [DSD: major depressive disorder (MDD) and/or dysthymic disorder (DD)] to determine whether these transient subthreshold manifestations later progress to a recognized BPSD. TMS are defined, for the purposes of this study, as manic-like symptoms of insufficient duration or number to warrant a diagnosis of BPSD, including standardized criteria for BP-NOS, similar to those used in the COBY study (5
). provides TMS diagnostic criteria. Two case presentations (using pseudonyms) below illustrate how TMS presented in this study.
Diagnostic criteria for transient manic symptoms (TMS)
Case study: 8-year-old girl
At baseline, Jane was diagnosed with attention-deficit hyperactivity disorder (ADHD), oppositional defiant disorder, separation anxiety disorder, and MDD+TMS. She recalled feeling intensely irritable several times in the previous two weeks without any trigger; the longest period lasted 30 minutes and she indicated that this was “the maddest” she had ever been. During these brief periods of intense irritability, she hit and bit other people. In addition, Jane’s mother reported brief periods wherein she seemed “too high for no apparent reason.” These lasted 1–2 hours/day for a few consecutive days. While in this “high” mood, Jane rapidly switched from topic to topic in conversation, and was caught grabbing her brother’s penis, and watching adult-rated sex scenes on DVDs in the family home. She was also “obsessed with her own breast development.” Jane converted to BP-I, most recent episode depressed at the six-month follow-up.
In this case example, Jane was noted to experience intense, but brief periods of irritability and elated mood, with accompanying racing thoughts and excessive involvement in pleasurable activities with high potential for painful consequences. However, their frequency and duration were brief, despite resulting in impairment, such that Jane did not meet criteria for BP-I, BP-II, BP-NOS, or cyclothymia.
Case study: 11-year-old boy
John was diagnosed at baseline with dysthymic disorder + TMS, ADHD, and conduct disorder. His grandmother and legal guardian, described periods in the past when John had devoted himself to unrealistic (and unsuccessful) goals, such as taking apart bicycles and fixing them as training to operate a bicycle repair business, or believing he was so strong that he could “beat up Arnold Schwarzenegger.” However, those were relatively fleeting occurrences and did not correspond with other symptoms of mania. In the week prior to the assessment, John reported having one day when he talked too fast and couldn’t be interrupted, but had no other accompanying manic symptoms. He also reported occasional nights where he didn’t feel he needed much sleep. John converted to BP-II at the 12-month follow-up.
In this case example, John had several isolated but vivid reports of grandiosity, decreased need for sleep, and pressured speech, but they were not of the frequency or duration nor were they accompanied by sufficient other manic symptoms that clustered during a unified time period to warrant a bipolar spectrum diagnosis.
Retrospective adult studies indicate that bipolar disorder with a prepubertal or adolescent onset is common among those diagnosed with this disorder and earlier age of onset is associated with a more pernicious course (7
). A majority of the respondents in these studies experienced impairing symptoms prior to receiving a bipolar disorder diagnosis. In one study, nearly three-quarters of participants reported experiencing one or more impairing manic symptom while diagnosed with unipolar depression (7
). This can pose a problem, as treatment with antidepressants may trigger mania (10
). Even though manic symptoms often manifest at a younger age, accurate diagnosis and treatment may be delayed by the clinician’s failure to consider such a diagnosis (8
Rates of conversion from unipolar depressive disorder to subsequent bipolar disorder in adults have ranged from 12.5% in an outpatient sample followed for 11 years (11
) to 45–50% for an inpatient sample followed for 15 to 23 years (12
). Clinical features associated with conversion include depression with psychotic features, a history of more than six depressive episodes, and a positive family history of mania.
Several prospective studies have assessed the rate and predictors of conversion to bipolarity in children and adolescents diagnosed with MDD (14
). Others have prospectively assessed adults with bipolar disorder who had prepubertal MDD (16
). These studies have found that conversion from MDD to BP-I and BP-II in prepubertal children and adolescents is relatively common, ranging from 20–49%, depending on the length of follow-up. Thus, diagnostic stability appears low for childhood-onset MDD (17
). Family history of bipolar disorder, rapid symptom onset, psychomotor retardation, mood congruent psychosis, and pharmacologically induced mania all have been identified as predictors of conversion. These studies have important clinical implications. First, children with MDD and their families should be alerted to the possibility of developing bipolar disorder and taught to recognize prodromal symptoms associated with mania (18
). Second, clinicians should be aware that children with MDD are at high risk for converting to bipolar disorder and should monitor them for emergent prodromal symptoms. Third, due to high rates of conversion, significant caution should be taken when prescribing antidepressants to children with MDD, as antidepressants may trigger childhood mania (10
). Finally, research to aid in predicting which children will convert to bipolar disorder after their index MDD episode is of vital importance to clinicians (11
Some studies have assessed prodromal symptoms and risk factors for childhood-onset bipolar disorder in high-risk youth (19
). Familial high-risk youth do not show classic symptoms of mania; instead, they show increased severity of depressed and irritable mood and problems with mood regulation. Very little is known about bipolar prodromes in young children.
No studies have assessed the rates of conversion to BPSD in children with DSD+TMS. Also, no studies to date have examined the influence of psychosocial treatments on subsequent conversion to BPSD. Studying rates of conversion from DSD to BPSD allows for the assessment of risk factors that can predict bipolarity. Thus, the aims of the present study were to determine rates of, and risk factors for, conversion in children with DSD+TMS over an 18-month follow-up period. The following hypotheses were employed:
Hypothesis 1: At baseline, children with DSD+TMS will have lower Children’s Global Assessment Scale (C-GAS) scores than children with DSD, but higher scores than children with BPSD.
Hypothesis 2: Children with DSD+TMS at baseline will convert to BPSD at follow-up at a higher rate than children with only DSD at baseline.
Hypothesis 3: Conversion rates will not differ as a result of participation in psychoeducational psychotherapy.
Hypothesis 4: Children with DSD+TMS at baseline who convert to BPSD at follow-up (converted group) will demonstrate greater impairment than those who do not convert (i.e., non-converted group) on the following baseline composite variables: clinical presentation, family environment, and family history.
Composite variables were used to reduce the number of analyses conducted in testing primary hypotheses. Secondary hypotheses were conducted to see which, if any, components of composite variables differed (clinical presentation: greater severity of prodromal manic symptoms, longer duration of prodromes, lower C-GAS scores; family environment: greater number of life events, more critical and hostile family environment; family history: higher rates of bipolar disorder diagnosis and symptoms for parents and second-degree relatives, higher rates of a loaded family history, and higher mood severity in the parent).