Although practicing in Australia, I have followed the PBD phenomenon in the USA for several years. PBD had become the most common diagnosis in pre-pubertal children in US psychiatric inpatient units by 2004 (Blader JC, Carlson GA, Biol Psychiatry 2007;62(2):107–114). “The epidemic of childhood bipolar disorder” (as later described by Allen Frances in Psychiatric Diagnosis Gone Wild: The “Epidemic” Of Childhood Bipolar Disorder, Psychiatric Times, April 8, 2010) was of interest to colleagues here in Australia when we became aware of it. Many US phenomena disseminate globally and we wondered if PBD would too.

Glen Spielmans, PhD (who, among other jobs, is the research editor for this newsletter’s sister publication, The Carlat Psychiatry Report), and I researched pharmaceutical industry documents released post-litigation that tell a sorry tale (Spielmans G & Parry P, J Bioethical Inquiry 2010;7(1):13–29). Among these documents was evidence of pharmaceutical companies seeking broadened criteria for bipolar disorder. (You can see the documents at http://bit.ly/UL9tJq) Internal pharmaceutical company documents noted that patents for SSRIs were expiring, whereas most atypical antipsychotics were young in their patent lives. Increasing bipolar disorder diagnoses was key to maximizing sales for on-patent antipsychotics. As Frances, chair of the DSM-IV task force, remarked: “New diagnoses in psychiatry can be far more dangerous than new drugs” (Frances A. Diagnosing the D.S.M. The New York Times. May 11, 2012).

PBD Generally Not Diagnosed Outside USA

It is true that if similar epidemiological methodology to the US researchers’ method is used, then comparable rates of PBD can be found outside the USA (Van Meter AR et al, J Clin Psychiatry 2011;72(9):1250–1256). There are PBD research centers in Europe, notably Spain, and in South America that have links with US researchers. But 17 years after the first publication in the USA about the postulated PBD phenotypes, PBD has not been accepted in mainstream clinical practice in other countries.

I was part of a group that surveyed the Royal Australian & New Zealand College of Psychiatrists (RANZCP) faculty of child and adolescent psychiatry (CAP) and found majority skepticism: only 3.5% thought our US colleagues were not overdiagnosing bipolar disorder, 90% thought they were overdiagnosing, and 6% were unsure (Parry P et al, Child Adolesc Mental Health 2009;14(3):140–147).

A German survey of child psychiatrists (Meyer TD et al, Bipolar Disord 2004;6(5):426–431), gave even more conservative results than our survey, and the British National Institute for Health and Clinical Excellence (NICE) 2006 guidelines on bipolar disorder stipulated that the PBD phenotypes were for research and not for use in clinical practice (NICE Clinical Guidelines 2006; www.nice.org.uk/CG38). A more recent German survey of inpatient diagnoses found a slight rise in bipolar diagnoses in late adolescence but no rise under age 15. They noted the contrast with US data: “While Blader and Carlson reported …73 children and 204 adolescents per 100,000 …the rates in Germany …are 0.14 and 5.22 per 100,000” (Holtman M et al, Bipolar Disord 2010;12(2): 155–163).

The international discrepancy in PBD diagnoses was reflected in three main child and adolescent psychiatry (CAP) association meetings in 2009: at AACAP in Hawaii there were more than 40 oral PBD presentations, whereas at both the RANZCP meeting in New Zealand and the large European Society for Child and Adolescent Psychiatry (ESCAP) meeting in Hungary there were none. At the International Association for Child and Adolescent Psychiatry and Allied Professions (IACAPAP) World Congress of CAP this year in Paris there was a debate: “Paediatric bipolar disorder, severe mood dysregulation or what?” where the widely discrepant international views were again apparent (learn more at http://bit.ly/TQh5r4).

So Why the Discrepancy?

From my perspective, PBD in the USA has arisen during a time when the biomedical paradigm has dominated. Quantitative data is valued over qualitative data with diagnoses based on structured interviews rather than multiple, less structured sessions with children and families. The US health system encourages “diagnostic upcoding” based on DSM diagnoses, which since DSM-III, have mostly been decoupled from psychosocial contexts. In addition, the pharmaceutical industry has exerted an unhealthy influence in research, medical education, and consumer awareness; and attachment and trauma factors are often overlooked (Parry P & Levin E, J Trauma & Dissociation 2012;13(1)51–68).

“Not Everything that Counts can be Counted and Not Everything that can be Counted, Counts”

This quote of Einstein’s is worth reflecting upon. The use of structured interviews/rating scales for diagnosing PBD has been criticized (Carlson GA, J Affect Disord 1998;51(2):177–187). Dr Stuart Kaplan gives a detailed critique in his book Your Child Does NOT Have Bipolar Disorder and on his Psychology Today blog of the same title (www.psychologytoday.com/blog/your-child-does-not-have-bipolar-disorder). In summary, the reliability and validity of the instruments are less robust than one might realize, with several points of ambiguity and interpretation that may lead to skewed results.

Beyond the USA, the mainstream view is that pre-pubertal mania is extremely rare to non-existent. This view is rooted in traditional phenomenology, attachment theory, psychodynamic theory, developmental psychology, family systems theory, and developmental trauma research. It is borne out in long term family therapy, intensive parenting training, dyadic parent-child post-trauma therapies, and play therapy. This is traditional clinical practice which finds biopsychosocial case formulations to be more informative than most DSM diagnostic labels.

Of course, many US clinicians still practice in the traditional way (for example Williams, Laurel L. Mental health and children. Los Angeles Times; December 14, 2008). There is mounting disquiet with the current DSM paradigm that has “atheoretical” diagnoses made with minimal regard to psychosocial context, as evidenced by an online petition (see http://bit.ly/UPPSrx).

PBD (and DMDD) Literature Overlooks Attachment and Trauma

I conducted a systematic literature review concepts such as attachment theory, post-traumatic stress, child abuse, maltreatment, and neglect in the PBD literature and found virtually nothing (see Parry PI. Paediatric Bipolar Disorder—Are Attachment and Trauma Factors Considered? In: Barnhill J, ed. Bipolar Disorder—A Portrait of a Complex Mood Disorder. InTech; 2012:165–190). The PBD literature focused on symptom clusters, rating scales, pharmacotherapy, genetics (though no clear answers), and neuroimaging (though no discernible reference to identical neuroimaging findings from the attachment-trauma literature). There was minimal mention of psychodynamic or family dynamic factors. A similar picture was evident in a brief review of the severe mood dysregulation/disruptive mood dysregulation disorder literature (Parry PI. Diagnostic Labels and Kids: A Call for Context. Clinical Psychiatry News; February 22, 2012).

Dr. Jennifer Harris has noted that developmental trauma/maltreatment was a factor for children erroneously diagnosed with PBD in a Boston inpatient unit (Harris J, Psychiatric Serv 2005;56(5):529–531). During my five years on an inpatient unit that serviced a whole Australian state, the youngest case of mania was aged 14. Colleagues since informed me of a 12-year-old pubertal boy with definite mania and a five-year-old girl who presented as quite manic and this aroused interest as a possible true pre-pubertal case—until it was noticed her manic symptoms appeared only when her mother was present. I saw one possibly manic seven-year-old boy, but his manic-defense coping mechanisms completely resolved after disclosure of sexual abuse and jailing of the perpetrator.

Trauma denial has a long history. Freud theorized about infantile libido on the basis of incredulity of child sexual abuse disclosures by his Viennese female patients. Abuse, pathogenic family dynamics and attachment insecurity are frequent amongst stressed families. The desire for a shame-free biological explanation and medication fix can be high.

Dr Edmund Levin describes how addressing underlying trauma, using developmental trauma disorder rather than PBD as a diagnosis, and appropriate staff training in two therapeutic residential units was useful in reducing medication prescriptions by 80% and violent incidents by 100% over a two-year period (Levin EC, J Am Acad Psychoanal Dyn Psychiatry 2009;37(3):519–538).

Additional Drivers of Diagnosis

Blader and Carlson argued that “diagnostic upcoding” had driven the rise in PBD because the US health system demands more serious diagnoses in order to get treated. No other developed nation has this health system driver for bipolar disorder. However, both Australia and Canada have similar drivers for autistic spectrum disorder and both have seen a clear uptick in diagnosis of ASD. (Skellern C et al, J Paediatr Child Health 2005;41(8):407–412; Thivierge J, NADD Bulletin 2008;XI(1):Article 2).

Much has been written elsewhere on the topic of pharmaceutical company influence. I’d like to note just one personal experience: A PBD researcher at AACAP 2009 was asked in the session why not call the children “affect dysregulated” rather than “bipolar.” The reply was frank: “If we don’t call them ‘bipolar,’ we won’t get funding.”

Final Comment

Practicing in Australia, I’ve yet to see any pre-teen cases of mania, and neither have most of my CAP colleagues. However I accept that rare true bipolar cases can occur in pre-pubertal children. For example, Carlson described a convincing case of a 10-year-old boy (Carlson GA, Am J Psychiatry 2009;166(1):18–24). That said, I invite my US colleagues to at least consider the diagnostic alternatives and cultural pressures before coming to the bipolar conclusion.