Although the presentation of BP in mid to late adolescence is considered similar to adult BP, the presentation of pediatric BP is debated. Many children have less than the 4–7-days duration specified in the DSM-IV-TR criteria for hypomania or mania, respectively. Pediatric BP is characterized by a predominance of mixed episodes and/or rapid cycling, irritability, chronicity with long episodes, and a high rate of comorbid attention-deficit hyperactivity disorder (ADHD) and anxiety disorder. The National Institute of Mental Health Research Roundtable on pubertal BP (2001) categorized pediatric bipolar phenotypes as “narrow” (DSM-IV-TR definitions of mania and hypomania) and “broad” (including the common clinical presentation of severe irritability, mood lability, temper outbursts, depression, anxiety, hyperactivity, poor concentration, and impulsivity). The diagnosis of BP should consider the developmental context in deciding what constitutes psychopathology. For example, increased self-esteem and goal-directed activity may be consistent with normal child development. Psychosis, most commonly auditory hallucinations, has been reported in 16–60% of youth with BP. The prevalence of psychosis is lower in adolescent mania than adult mania.
In summary, it is difficult to diagnose pediatric BP because of the variability in the clinical presentation, high comorbidity, and symptom overlap with other psychiatric disorders, the role of development in symptom expression, the difficulty experienced by children in reporting their symptoms, and social context in which the BP is developing (e.g., family conflicts). However, evidence is emerging that pediatric BP is a spectrum disorder (from BP Not Otherwise Specified [NOS] through BP-I) with a consistent course and outcome.
Although psychological testing is not involved in the diagnosis of BP, BP often is associated with cognitive deficits in children and adolescents. A study by Dickstein and Leibenluft using the computerized Cambridge Neuropsychological Test Automated Battery (CANTAB) reported difficulties in attentional set shifting and visuospatial memory in pediatric BP. A study by McClure and Leibenluft comparing children with BP to children with anxiety disorders and healthy controls showed that children with BP misinterpreted sad, happy, and fearful child faces as angry as compared with anxious and healthy groups. Interestingly, children with BP did not misinterpret adult faces.
No specific laboratory findings are diagnostic of BP in children and adolescents.
Although much new research exists on neuroimaging, most of the studies are preliminary. Structural magnetic resonance imaging (MRI) studies suggest that white matter hyperintensitites in both cortical and subcortical brain regions and smaller amygdalar size are correlated with pediatric BP. In addition, smaller parietal and temporal lobe cortical gray matter, bilateral and left sided reductions in amygdala size, and bilateral decrease in hippocampal volume have been noted in pediatric BP. Studies have also indicated reduced gray matter volume in the dorsolateral prefrontal cortex (DLPFC). Bilateral larger basal ganglia, particularly an increase in putamen size, was identified in adolescent BP. Functional MRI studies show increased left thalamus and putamen activation and both cortical and subcortical dysfunction.
Preliminary proton magnetic resonance spectroscopy studies have suggested that substances which are markers for neuronal integrity such as N-acetyl-aspartate, choline, myoinositol, and creatine/phosphocreatine are affected in the fronto-striatal region, cingulate cortex, DLPFC, and other areas of the brain. These results are preliminary because they include small sample size and subjects in various phases of illness (e.g., depressed, hypomanic, euthymic). In addition, many subjects had comorbid disorders and were taking medication, which may have confounded the findings.
Retrospective studies and naturalistic longitudinal studies of children and adolescents with BP report that 40–100% will recover, within 8 consecutive weeks, without meeting criteria for mania, hypomania, depression, or a mixed affective state, 1–2 years later. Of patients who recover, 60–70% show recurrence of symptoms within 10–12 months with hospitalization, psychosis, suicide attempts and completion, and poor psychosocial functioning.
As there is controversy over the presentation of pediatric BP, it is useful to study the course of the full spectrum of BP phenotypes. A recent study lead authored by Birmaher (2006) followed BP spectrum disorders (BP-I, BP-II, and BP-NOS). BP-NOS is defined as (1) elated mood plus two DSM-IV-TR BP symptoms or irritability plus three DSM-IV-TR BP symptoms; (2) at least 4 hours of symptoms in a 24 hour period; and (3) of 4 days lifetime total of symptoms. This study found that, compared with BP-I adults, BP-I youths spend significantly more time symptomatic with more mixed/cycling episodes, mood symptom changes, and polarity switches. A significant 25% of BP-NOS subjects converted to BP-I or BP-II. Furthermore, 70% of subjects with BP recovered from the index episode whereas 50% had at least one syndromal recurrence, most commonly a depressive episode. During follow-up, for 60% of the time, subjects had syndromal or subsyndromal symptoms with many changes in symptoms and shifts of polarity. Three percent of the subjects experienced psychosis. Twenty percent of BP-II subjects coverted to BP-I. Early onset, BP-NOS, long duration of mood symptoms, low-socioeconomic status, and psychosis were associated with poorer outcomes and rapid mood changes.
At this time, although suggested by familial transmission, it is not clear that pediatric BP is continuous with adult BP. In a community-based, adolescent longitudinal study, 5.7% of patients with abnormal mood, defined as persistently elevated, expansive, and irritable mood, did not go on to meet full DSM-IV-TR criteria of BP by the early twenties. In a retrospective interview of a large sample of individuals with adult BP, approximately 30% reported the onset of symptomatology before 13 years of age and approximately 40% during 13–18 years of age.
Earlier onset BP symptoms are associated with greater rates of anxiety and substance-abuse disorders, more recurrence, more rapid mood changes, shorter periods of euthymia, a higher incidence of suicide attempts, violence, and a history of abuse.
Depressed children and adolescents are at increased risk (10–20%) of developing BP, particularly if they present with psychotic symptoms, develop hypomania in response to pharmacological treatment of depression, and have a strong family loading for BP.