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Early Onset Schizophrenia: Diagnostic Dilemmas and Treatment Challenges

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Early Onset Schizophrenia: Diagnostic Dilemmas and Treatment Challenges REVIEW Early onset schizophrenia: diagnostic dilemmas and treatment challenges Jennifer Cheng Early onset schizophrenia (EOS), which is defined as onset prior to 18 years of age, is Shannon†1 and associated with significant morbidity, chronicity and psychosocial impairment. EOS appears Jon McClellan2 to be both clinically and neurobiologically continuous with the adult-onset form, although †Author for correspondence 1University of Washington, there are some important differences. Although the treatment literature specifically Department of Psychiatry, addressing juveniles with schizophrenia is sparse, the adult literature appears to apply, Box 356560, Seattle, WA given appropriate developmental considerations. Given the significant morbidity, chronicity 98195, USA Tel.: +1 206 543 6577 and psychosocial impairment associated with EOS, it is imperative that clinicians are familiar [email protected] with the phenomenology, diagnosis, clinical course and treatment of this disorder. This 2Children's Hospital and article provides a brief description of EOS with a focus on treatment modalities, including a Regional Medical Center detailed review of psychopharmacologic and psychotherapeutic interventions. PO Box 5371/M1-1 Seattle, WA 98105, USA Tel.: +1 206-987-2760 [email protected] Early onset schizophrenia (EOS) (defined as onset psychotic disorders. However, other psychopa- prior to age 18 years) is diagnosed using the same thologists, such as Bender and Kanner, placed criteria as for adults and appears to be both clini- it within broader categories defined by devel- cally and neurobiologically continuous with the opmental deficits in language, social relations, adult-onset form. Unfortunately, it is often a more perception and movement. Therefore, child- severe form of the disease and is associated with hood psychoses often included a broader cate- significant morbidity, chronicity and psychosocial gory of neurodevelopmental disorders, impairment. There are also considerable differ- including autism. It was the work of Kolvin [1] ences between demographic factors, clinical pres- and Rutter [2] who demonstrated that EOS entation and long-term outcome of EOS as was a specific entity, similar to adult schizo- compared with adults. phrenia. In the 1970s, DSM-III revised the The study of EOS is important for several rea- criteria so that EOS was diagnosed using the sons. This subgroup of patients may share a same criteria as those used for adults. higher degree of homogeneity and in as much are an important population in which to study sus- Epidemiology pected etiologic factors. Since the illness disrupts Given the rarity of EOS, few studies have exam- neurodevelopmental processes in the growing ined the incidence rates in the population. child, important information may be gleaned by However, available evidence suggests the preva- examining the onset and progression of the illness lence of schizophrenia in children is signifi- against the backdrop of normal development. cantly lower than in adults, which is estimated Moreover, EOS is often a debilitating disorder at approximately 1% [3]. The onset rate rises that can have a particularly deleterious effect precipitously during the age range of 15 to upon cognitive and social functioning. There- 30 years [3]. Onset prior to the age of 12 years is fore, efforts to improve the impact of therapeutic very rare. In early onset samples, males tend to interventions are critical. It is imperative that cli- predominate [4]. Thomsen found that, in a nicians working with the young are familiar with study of all youths hospitalized for schizophre- Keywords: the phenomenology, diagnosis, clinical course nia in Denmark over a 13-year period (n = atypical antipsychotics, early and treatment of this disorder. This article will 312), only four were under the age of 13 years onset schizophrenia, psychosis give a brief description of EOS with an emphasis and only 28 were younger than 15 years of age on treatment modalities. [5]. EOS, especially in those under the age of 13 years, occurs predominantly in males, with Background ratios of approximately 2:1 [1,6–10]. The validity Historically, EOS was originally characterized of the diagnosis in preschoolers is questionable as being similar to schizophrenia in adults, given developmental challenges in discerning Future Drugs Ltd dating back to Kraeplin’s initial descriptions of true psychotic symptoms. 2004 © Future Drugs Ltd ISSN 1475-0708 http://www.future-drugs.com Therapy (2004) 1(1), 131–147 131 REVIEW – Shannon & McClellan Etiology & pathogenesis Approximately 30% of people with this deletion Schizophrenia is currently thought to be a com- develop symptoms of psychosis [16,17]. Although plex disorder with polygenic, multifactorial etiolo- cases of 22q11 deletion are over-represented in a gies. Three primary areas of focus have been study of childhood-onset schizophrenia (COS) identified in the adult literature thus far: genetics; [18], an earlier age of onset was not associated viral exposure; and neurodevelopmental insults. with the deletion in a large screening study [19]. It is important to remember however, that Nicolson and colleagues found that parents of mechanisms may not necessarily have a causal patients with COS had a significantly higher relationship and that schizophrenia continues morbid risk of schizophrenia spectrum disorders to be viewed as a complex syndrome without a than parents of patients with adult-onset schizo- single etiology. Given the lack of research spe- phrenia (AOS) (24.74 vs. 11.35%) [20]. This is cifically focusing on the etiologies of EOS, the consistent with findings by the UCLA-NPI group data presented is what is currently known about [21], which continue to provide convincing evi- schizophrenia in the general population. When dence for the hypothesis that there is a continuous available, studies specifically examining EOS etiology between COS and AOS. will be noted. Despite these promising findings, there is not one single specific gene or chromosomal region Genetics that has been consistently found across studies to There is substantial evidence that genetics play be definitively associated with schizophrenia. an important role as a risk factor for the develop- Given schizophrenia’s heterogeneity, it is likely ment of schizophrenia with a heritability rate of that the genetic component of the disorder is approximately 80% [11]. The lifetime risk of much more complex than identifying a single developing schizophrenia is 5–20 times higher in gene. Moreover, there may be other types of first-degree relatives of affective probands when mechanisms, such as epigenetic influences, yet to compared with the general population [12]. Posi- be identified that relate to the development of tive family histories of schizophrenia are noted in the disorder. youths with EOS, although whether the relative risk is the same as adults has not been well stud- Neurodevelopmental theory ied [4]. Despite this evidence, no single model of The neurodevelopmental hypothesis of schizo- genetic inheritance has yet been identified. The phrenia is based on the idea that early central nerv- phenotype of schizophrenia is heterogeneous ous lesions affect normal maturational processes. and it is likely that multiple genes are involved. Evidence supporting this theory is partly based on Moreover, the risk conferred may not always be premorbid impairments seen in childhood and expressed as schizophrenia but rather as related adolescence of those who later develop schizophre- traits, such as a schizoid personality. Finally, nia and may represent the neuropathologic mani- many cases are assumed to be sporadic and per- festations of the disorder. Kolvin’s work in the haps due to complicated gene–environment 1970s showed that 87% of 33 children with the interactions. Numerous linkage and candidate equivalent of EOS were premorbidly odd and had genes studies have been completed to date. developmental delays, mostly in speech [1]. Multi- There are several chromosomal regions that at ple recent studies have also replicated delayed least one study has associated with schizophre- motor milestones, speech problems, lower educa- nia, including 1q, 5p, 5q, 6p, 6q, 8p, 10p, 13q, tional test scores and/or poor social adjustment 15q and 22q [13]. Another study identified these before the onset of the disorder [22–25]. A recent genes as well as 18p, although the precise linkage study suggests that these deficits may be more rele- in schizophrenia has yet to be established [14]. vant to those with adolescent onset of the disorder Genes of interest include dybindin (6p22), neu- [26]. In the adult literature, perinatal complica- regulin (8p22) and catechol-O-methyltransferase tions, alterations in brain structure and size, minor (COMT) (22q11) [15]. COMT is of particular physical anomalies and disruption of fetal neural interest because it is found in the commonly development, particularly during the second tri- deleted region of chromosome 22 that is associ- mester of pregnancy, have been correlated with the ated with velo-cardio-facial syndrome (VCFS), illness [27–29]. although there are other genes of interest in this region as well. VCFS is a genetic disorder charac- Infectious processes terized by palatal, facial, cardiac, congenital Viral exposure has been implicated as a risk factor abnormalities and psychiatric conditions. for schizophrenia. Individuals with schizophrenia 132 Therapy (2004) 1(1) Early onset schizophrenia – REVIEW are more likely
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