Interventions For Highrisk Children

A major goal of studying children of persons with schizophrenia has been to develop screening and intervention tools. Such efforts are in their infancy, with the first early intervention study being initiated by Falloon [92] slightly over a decade ago. Genetic testing for children who may be at risk would be one means of early detection, although this information alone would not be sufficient and the specific genes involved have not yet been identified [93]. Furthermore, using genetic information for early detection is replete with ethical ramifications that are still being considered in the public arena. Another option would be to identify a set of prodromal symptoms and use those as a means of detecting at-risk individuals. MMler and Husby [94] identified two prodromal symptoms, ''disturbance in self-perception'', which is characterized by a sense of detachment or unreality, and ''extreme preoccupation by and withdrawal to overvalued ideas''. These symptoms may be useful in detecting at-risk persons. These experiential features were manifested in a number of behavioural dimensions, including quitting school or work, or major absenteeism; significant, observable shift in interests; social passivity and isolation; and marked and lasting changes in global appearance or behaviour [94]. Finally, identifying biobehavioural markers or indicators has yielded a rich body of literature but, with the exception of some neuropsychological findings, none of the identified markers offers the degree of sensitivity, specificity and predictive power needed for a useful screen.

A few intervention efforts have recently been launched, often based on the notion that shorter duration between first psychotic episode and subsequent treatment is associated with a better prognosis [95,96]. Improved access to care and increased education efforts have been shown to reduce treatment delay [95]. Other intervention options include pharmacological treatment with antipsychotics initiated during the prodromal phase or perhaps earlier. The risks of such intervention are significant: children may be more prone to side effects, including dyskinesias, and need careful monitoring [97]. The benefits of administering these medications, based on the possibility that they may develop schizophrenia, would need to be carefully weighed against the potential risks. Cornblatt's data from the Hillside Recognition and Prevention Project indicates that antidepressants in combination with a mood stabilizer and/or anxiolytic were as effective as antipsychotics in yielding clinical improvements among high-risk individuals [98]. One benefit of such an approach is that these medications have fewer negative side effects as compared to antipsychotics. Other intervention strategies include individual, group or family psychotherapy. For example, behavioural family therapy that includes education, communication skills training and problem solving has been shown to be helpful. Also effective is a group format that includes patients' relatives and addresses issues of problem solving, communication and expectations [99]. Finally, a controversial strategy proposes that family planning interventions be employed to prevent pregnancy in chronically ill female patients [100].

Although several early detection and intervention efforts have yielded promising results, as noted previously, they have also generated some controversy. Verdoux and Cougnard [101] note that there is no solid evidence that the duration of untreated psychosis is causally related to poor outcome. They also indicate that the threshold for who is actually in need of early intervention is unclear, as is the target population [101]. Data from high-risk studies might be useful in addressing some of these concerns. The Hillside Recognition and Prevention Program, which was launched in 1998, suggests that schizophrenia is preceded by a cluster of neurocognitive deficits, with actual psychosis emerging much later initially in the form of positive symptoms [98]. Based on findings from high-risk studies and the neurodevelopmental model, Cornblatt and the Hillside researchers [98] have identified a clinical entity that includes cognitive, academic and social impairments as well as disorganization and odd behaviour (CASID). If conclusions from genetic high-risk studies are correct - that early neurocognitive deficits play a causal role in schizophrenia - then Cornblatt [98] suggests that intervention efforts should be directed toward treating these deficits rather than waiting for prodromal symptoms to emerge. Mirsky and Duncan [102], Walker and Hochman [103] and others have made the same point in a recent volume on early intervention and prevention in schizophrenia [104].


We have reviewed the empirical literature on children of persons with schizophrenia, and have identified characteristics of such children that may qualify them as candidates for behavioural, environmental or pharmacological intervention. We have not yet found a biological marker that is unique to schizophrenia, and we must still begin our triage by asking whether there is a first-degree relative of the child with the disorder. From that point of view, we may not be much better off than Koller in 1895 or Kraepelin in 1907 [10,11]. Nevertheless, we now have well-controlled studies implicating genetic factors in the transmission of schizophrenia [14,15]; moreover, there are a number of candidate genes which we believe confer susceptibility to the disorder, including locations on chromosomes 6p, 8p and 11q [16-18]. A location in chromosome 6p (21.3) is of special interest to us, because a number of disorders in which impaired attention is a prominent symptom (schizophrenia, narcolepsy, attention-deficit/hyper-activity disorder, juvenile myoclonic epilepsy) have an abnormal gene in this HLA (human lymphocyte antigen) region of the chromosome [105].

Although most of us no longer believe in the concept of the schizo-phrenogenic mother or family, we can appreciate the impact of harsh treatment within the family [8] or from the community [39] on the severity of the disorder in a child at risk. So perhaps Fromm-Reichmann was not entirely wrong [55]. In addition, we now have superior behavioural methods (i.e. sophisticated assessments of attention, memory and motor skills) of identifying the one-in-ten at-risk child who is actually likely to develop a disorder. We know that we must proceed with some caution with respect to attention deficits, as there are other disorders in which compromised attention is seen [105].

Clearly, our progress in identifying a marker for schizophrenia is ultimately dependent upon our understanding the aetiology of the disorder, or disorders, that comprise the schizophrenia spectrum. As a potential contribution to the search for that holy grail (or grails) [104], we offer the modest suggestion that the final truth must implicate pathophysiological mechanisms in the brainstem, a main support of sustained attention [103].

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