A greater understanding of how the brain works, including the effect of environment on it development, has led to advances in diagnosing and treating psychopathology. The latest findings will be presented at an international meeting, along with a discussion of how much work is to be done and the great need for qualified child psychiatrists, especially in developing countries.
The European Society for Child and Adolescent Psychiatry (ESCAP), which was founded in 1954 to foster bonds between those working in the field throughout Europe, met in Paris from Sept. 28 to Oct. 1. The focus this year was on developmental psychopathology, chosen to highlight the enormous advances our understanding of human behavior can make when developmental processes from conception through adolescence become the focus of both clinical and laboratory study. This approach began on two fronts, first with naturalistic and epidemiological investigations in England by Jack Tizard, Michael Rutter, M.D., and Philip Graham, both in normal populations and among children with autism and children reared in institutions. Then later, developmental psychologists applying laboratory techniques joined forces with psychoanalytic researchers in the United States and Switzerland focusing on newborns and their mothers. They found very different trajectories in normal and pathological development than was the accepted clinical wisdom. Much of this research found its way into ESCAP's journal.
In this year's program, many papers addressed the incredible advances in the genetic aspects of illness while recognizing that the relationship between genetic predispositions and the modes of expression of a particular disorder depend not only on the stage of development of the child, but also on the social context in which the child exists. Particular aims of this conference were to examine the boundaries between normality and pathology and the nature of the expression of enduring behaviors in a child that, in turn, "create" an environment that can engender pathogenicity in its own right. This new environment, in part created by the child, can reorganize the personality and have long-lasting effects removed from the etiology of the initial behavior.
For decades, the direction of causality has been confused by missing the effect of a child's behavior on their environment. Autism is a prime example. Further, it is clear that some of our thinking about psychopathology clouded our ability to see. For example, we have now come to recognize that manic-depressive illness in children is not rare. Great delays in recognizing disorders in children have occurred in part because the diagnostic manuals have either ignored their specialness or applied criteria to children as if they were little adults. Nowhere is this more apparent than in the diagnosis of posttraumatic stress disorder in young people, and especially in the very young child.
Today's challenges are how to integrate this new data coming from so many disparate disciplines (e.g., neuro-imaging, genetics, cognitive sciences and pharmacology) and how to make a shift in our thinking about therapeutic approaches without--in the excitement--losing the advances made in prior decades (Westen, 1999). Many presentations at the ESCAP conference focused on this dialectical interface.
Insights Into Brain Activity
Studies presented at the conference attempted to define early precursors of a later onset of a disorder. For example, symptoms of cognitive decline appear early in children at high risk for developing schizophrenia (Fuller et al., 2002). Studies underway in the United States, England and Australia are finding that the cognitive losses can be stemmed with preventive medication (McFarlane et al., 2003; McGlashan et al., 2003). Treating children at risk with medication raises ethical issues, but the results are very promising. It remains to be seen if this approach can prevent the devastating effects on the brain and the disorder itself.
There has been an enormous--though quietly heralded--paradigm shift in the way we think about psychopathology. To start, the brain is no longer seen as static. Stress produces effects on areas of the brain, such as the hippocampus, through an outpouring of cortisol and other glucocorticoids in which neurons are actually lost (Bremner, 2002). The hippocampus not only affects memory, but may be a nodal point in the production of depression. Through stimulation of brain-derived neurotrophic factor (BDNF), neurons can actually regenerate in the hippocampus (Kojima et al., 2001; Larsson et al., 2002). In young boys with PTSD, diminished brain volume can be demonstrated (De Bellis and Keshavan, 2003).
Neuroimaging studies have found increased activation in the amygdala after a PTSD response was provoked (Hull, 2002). The amygdala--among other functions--is the early/automatic warning system of danger. It may function "hyperactively." In children with autism, this may cause increased head growth. Simon Baron-Cohen has suggested that the neurons that differentiate boys' and girls' brains may be causing what some see as an exacerbation of the tendency of boys to be systematizers rather than empathizers--as girls are found to be. In his laboratory, newborn girls have been found to prefer faces more than mechanical mobiles, which newborn boys pay more attention to. Three-year-old girls have been found to be more competent at picking up the interpersonal issues in a story.
In patients with bipolar disorder, studies have found a substantial loss of gray matter, which may be prevented by the use of lithium (Eskalith, Lithobid) and/or valproate (Depakote) (Manji et al., 2000). In depression, BDNF is stimulated by antidepressants to cause neuronal development (Shimizu et al., 2003). These may be important arguments for early pharmacological intervention in children, although studies must be balanced by controls in whom stress reduction and its effect on brain development are measured. We know that adult women who have been abused early in life put out six to seven times the amount of cortisol when placed in a neutral, but stressful, situation (e.g., solving math problems) (Westen, 1999). There is further suggestion that those who suppress this early trauma are even more prone to react to stress with an outpouring of stress hormones.
Advances in Cognitive Understanding
The cross-fertilization from psychology has been amazingly rewarding, and serendipity abounds. The discovery of the cognitive bases for some of the behaviors in autism, such as difficulties with "theory of the mind tasks," led to studies using psychiatric controls (Buitelaar et al., 1999). One tantalizing initial finding is that children with attention-deficit/hyperactivity disorder may have similar difficulties understanding the inner thoughts of another along with the problems they have in areas of so-called executive functioning (Booth et al., 2003; Dyck et al., 2001; Sergeant et al., 2002). Children with ADHD may also have trouble reading the emotions in others because they struggle with facial and voice recognition tasks. Children with conduct disorders have also been found to do more poorly than controls, but appear to make consistent mistakes (i.e., mistaking happiness and fearfulness for anger) (Cadesky et al., 2000).
There has been a huge movement forward in our understanding of conduct problems in children, based on collaborative studies from England, Australia and Sweden. Epidemiology studies done in Sweden found that about 5% of children will be responsible for more than 60% of adult criminal behavior (Stattin and Magnusson, 1996). Recognizing the differences between lifelong conduct problems and adolescent-limited conduct disorder has been enormously enhanced by these studies. The physiology of conduct problems has given a great boost to identifying children before they get into trouble. The goal is to provide these children with environmental input that will prevent their developing behavioral difficulties.
Slow pulse rate in 3-year-olds has been found to be a robust predictor of which children will exhibit behavioral and aggressive problems eight years later (Raine, 2002). Slow pulse rate continues to be a strong predictor of adult aggressive criminal behavior when many confounding variables are factored out. Since nicotine appears to reduce the pulse rate, this may explain the association of the strong effect of smoking on the fetus and later antisocial behavior (Raine, 2002). This author suggested that it may "reflect reduced noradrenergic functioning and a fearless, stimulation-seeking temperament." Using a developmental framework to describe evidence of prefrontal lobe dysfunction, Raine opined that the late adolescent with such dysfunction will be overtaxed by the social and executive function demands of entry into the adult world, leading to an inability to control antisocial tendencies.
Perinatal difficulties are associated with risk for antisocial behavior, but only when combined with adverse psychosocial risk factors (e.g., the mother's lack of caring for her infant). There are studies underway to look at the effects of cortisol production and normal children's autonomic reactivity on their brains, which may have some use in understanding susceptibility to physical illnesses (Boyce et al., 1995).
This interplay is the stuff that child psychiatry is made of, and what the ESCAP conference aimed to address. The findings obviously require the utmost care and must be used in only the most beneficial and therapeutic ways.
Developmental psychopathology brings a degree of complexity and difficulty to the tasks of the practitioner that is no less than the excitement it generates. From advances in the study of children with autism and the neuropsychological findings comes a better recognition of children who were passed off as unpsychologically minded or "nerdy." These socially inept children are found to be among those who have cognitive profiles in which their language appears superior, but their pragmatic language is such that they do not read others well. They are often seen as lacking empathy, where in reality they lack the cognitive underpinnings that make for empathy. These are not children with Asperger's syndrome, but they have similar deficits. From an understanding of these deficits, we have begun in our region to develop specific group and school approaches for these children with so-called nonverbal learning disabilities. Traditional forms of psychotherapy practiced by someone aware of the cognitive difficulties of these children can also help with issues of self-esteem.
While this very sophisticated interaction between cognitive psychology, brain imaging, genetics, and neurochemical and psychopharmacological study is going on, there are still countries in Europe with no or only a handful of child psychiatrists. The World Health Organization and some private foundations are attempting to help seven countries emerging from decades of neglect and poverty develop plans for the delivery of mental health care.
I have been consulting in Albania over the past five years, helping establish a program in child psychiatry (Schreier, 2000). Unlike the usual image the mention of countries like Albania or Bulgaria might call up, I have found an extremely educated and highly motivated group of colleagues to work with. Nongovernmental organizations have not provided the kind of funding needed to get programs off the ground in child mental health care in particular, nor is there a deep understanding among the country's politicians of the need for continued funding.
In Tirana, Albania, for example, where there is a newly refurbished pediatric hospital rebuilt by the European Union and equipped by the Japanese and the Swiss, there is a competently trained group of pediatric residents eager for more training in child development and psychiatry. We have defined a program in which, after a year of pediatric residency, a student can take two years of training in child development and begin practice in that subspecialty. There are no developmental or behavioral pediatricians in Albania at this time. If students then choose, they can take two years of child psychiatry training and begin practicing in that field. These are different standards than one would find in Western Europe or the United States, but they address a local need and, in many ways, the child psychiatrist will have more training in development than fellows in the United States now receive. Indeed, there is a movement underway to make it easier for pediatricians to train in child psychiatry here in the United States.
The differences between child psychiatry now and three decades ago can be found in conferences such as the ESCAP. We are still left with the enormity of putting into practice all that we have learned. This is painfully true in the United States and Western Europe. But in some countries, just a single subscription to a journal that describes this knowledge is still a luxury.
Booth R, Charleton R, Hughes C, Happe F (2003), Disentangling weak coherence and executive dysfunction: planning drawing in autism and attention-deficit/hyperactivity disorder. Philos Trans R Soc Lond B Biol Sci 358(1430):387-392.
Boyce WT, Chesney M, Alkon A et al. (1995), Psychobiologic reactivity to stress and childhood respiratory illnesses: results of two prospective studies. Psychosom Med 57(5):411-422.
Bremner JD (2002), Structural changes in the brain in depression and relationship to symptom recurrence. CNS Spectrums 7(2):129-139.
Buitelaar JK, van der Wees M, Swaab-Barneveld H, van der Gaag RJ (1999), Theory of mind and emotion-recognition functioning in autistic spectrum disorders and in psychiatric control and normal children. Dev Psychopathol 11(1):39-58.
Cadesky EB, Mota VL, Schachar RJ (2000), Beyond words: how do children with ADHD and/or conduct problems process nonverbal information about affect? J Am Acad Child Adolesc Psychiatry 39(9):1160-1167.
De Bellis MD, Keshavan MS (2003), Sex differences in brain maturation in maltreatment-related pediatric posttraumatic stress disorder. Neurosci Biobehav Rev 27(1-2):103-117.
Dyck MJ, Ferguson K, Shochet IM (2001), Do autism spectrum disorders differ from each other and from non-spectrum disorders on emotion recognition tests? Eur Child Adolesc Psychiatry 10(2):105-116.
Fuller R, Nopoulos P, Arndt S et al. (2002), Longitudinal assessment of premorbid cognitive functioning in patients with schizophrenia through examination of standardized scholastic test performance. Am J Psychiatry 159(7):1183-1189.
Hull AM (2002), Neuroimaging findings in post-traumatic stress disorder. Systematic review. Br J Psychiatry 181:102-110.
Kojima M, Takei N, Numakawa T et al. (2001), Biological characterization and optical imaging of brain-derived neurotrophic factor-green fluorescent protein suggest an activity-dependent local release of brain-derived neurotrophic factor in neuritis of cultured hippocampal neurons. J Neurosci Res 64(1):1-10.
Larsson E, Mandel RJ, Klein RL et al. (2002), Suppression of insult-induced neurogenesis in adult rat brain by brain-derived neurotrophic factor. Exp Neurol 177(1):1-8.
Manji HK, Moore GH, Chen G (2000), Clinical and preclinical evidence for the neurotrophic effects of mood stabilizers: implications for the pathophysiology and treatment of manic-depressive illness. Biol Psychiatry 48(8):740-754.
McFarlane WR, Pollack DA, McGorry PD et al. (2003), Early intervention in psychosis: where science meets community psychiatry. Symposium 39. Presented at the 156th Annual Meeting of the American Psychiatric Association. San Francisco; May 20.
McGlashan TH, Zipursky RB, Perkins D et al. (2003), The PRIME North American randomized double-blind clinical trial of olanzapine versus placebo in patients at risk of being prodromally symptomatic for psychosis. I. Study rationale and design. Schizophr Res 61(1):7-18.
Raine A (2002), Annotation: the role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children. J Child Psychol Psychiatry 43(4):417-434.
Schreier H (2000), Child and adolescent psychiatry: European culture. American Academy of Child and Adolescent Psychiatry News 31:218-222.
Sergeant JA, Geurts H, Oosterlaan J (2002), How specific is a deficit of executive functioning for attention-deficit/hyperactivity disorder? Behav Brain Res 130(1-2):3-28.
Shimizu E, Hashimoto K, Okamura N et al. (2003), Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants. Biol Psychiatry 54(1):70-75.
Stattin H, Magnusson D (1996), Antisocial development: a holistic approach. Development and Psychopathology 8:617-645.
Westen D (1999), The scientific status of unconscious processes: is Freud really dead? J Am Psychoanalytic Assoc 47(4):1061-1106.