Clinical phases of schizophrenia
Premorbid social and developmental impairments
Child and adolescent onset schizophrenia is characterized by poor premorbid functioning and early developmental delays (Alaghband-Rad et al. 1995; Hollis 1995). Similar developmental and social impairments in childhood have been reported in adult onset schizophrenia using population-based cohorts free from referral biases (Done et al. 1994; Jones et al. 1994; Jones & Done 1997; Malmberg et al. 1998). While age of onset comparisons are plagued by methodological difficulties, premorbid developmental impairments appear to be more common and severe in the child and adolescent onset forms of the disorder.
Hollis (1995) in a retrospective case - control chart study of 61 cases of child and adolescent onset schizophrenia (aged 7 - 17) reported significant impairments in language development (23%), motor development (31%) and social development (36%). Developmental impairments were most common in cases with onset of schizophrenia before age 13 years. Hence, a history of premorbid impairments appears to be most common in the very earliest onset cases. Nicholson et al. (2000) reported significant premorbid speech/language, motor and social impairments in 50% of childhood onset patients with onset of psychosis before the age of 12 years. In comparison, language and motor developmental delays are reported in only about 10% of individuals destined to develop schizophrenia in adult life (Jones et al. 1994).
A consistent characteristic in the premorbid phenotype is impaired sociability. In child and adolescent onset schizophrenia, about one-third of cases have significant difficulties in social development affecting the ability to make and keep friends (Hollis 1995). Similar, but less frequent difficulties with premorbid sociability have been noted in representative population samples of adult schizophrenia (Malmberg et al. 1998). Interestingly, the Hollis study (1995) indicated that some cases would have met diagnostic criteria for Asperger syndrome, schizotypal personality disorder or atypical autism prior to the onset of psychosis
In the National Institute of Mental Health (NIMH) study of childhood onset schizophrenia, 34% of cases demonstrated transient symptoms of pervasive developmental disorder during the premorbid period (Alaghband-Rad et al. 1995).
Premorbid IQ appears to be lower in child and adolescent onset schizophrenia than in the adult form of the disorder. The mean premorbid IQ lies in the mid to low 80s, 10 - 15 IQ points lower than in most adult studies (R. Asarnow et al. 1994; Spencer & Campbell 1994; Alaghband-Rad et al. 1995). In the Maudsley study (Hollis 1999) one-third of child and adolescent onset cases had an IQ below 70 (mild learning disability range).
One interpretation of these findings is that a subgroup of adolescent schizophrenic cases has abnormal premorbid development with the rest developing normally. In fact, careful analysis shows that there is no abnormal developmental subgroup - this is simply an artefact of using rather crude categorical measures of premorbid development. Continuous IQ measures show that the whole distribution of IQ is shifted down compared with both adolescent affective psychoses and adult schizophrenia.
These findings are consistent with the view that premorbid impairments are manifestations of a genetic/developmental liability to schizophrenia. It seems clear that the premorbid phenotype does not just represent non-specific psychiatric disturbance. Subtle problems of language, attention and social relationships are typical while, in contrast, conduct problems are rare. However, premorbid social and behavioural difficulties are not specific to schizophrenia. Premorbid deficits also occur in adolescent affective psychoses, at a lower rate than in schizophrenia but higher than in non-psychotic psychiatric controls (van Os et al. 1997; Sigurdsson et al. 1999).
Significance of premorbid impairments: a risk factor or precursor of psychosis?
Premorbid impairments could lie on a causal pathway for psychosis or, alternatively, they could be markers of an underlying neuropatholgical process, such as aberrant neural connectivity which may be the cause of both premorbid social impairment and psychosis. Causality is clearly implicit in ideas of primary prevention and the risk estimates provided by population-based epidemiological studies of prepsychotic impairments (Done et al. 1994; Jones et al. 1994; Malmberg et al. 1998). Frith (1994) speculated on the possible cognitive mechanisms that might link deficits in social cognition or ‘theory of mind’ in a causal pathway to both positive and negative psychotic symptoms. If these characteristics are causally related then modifying the ‘primary’ cognitive or social deficits should reduce the risk of psychosis. Alternatively, cognitive and social deficits, although often present, may not be necessary in the pathogenesis.
The fact that individuals can develop schizophrenia without obvious premorbid impairments supports this view. In these circumstances, an intervention aimed at the neurobiological level (e.g. antipsychotic medication) may be necessary. Only a high-risk longitudinal intervention study can adequately address the issue of causality, and this would clearly require an intervention that had benefits for the majority of individuals with the premorbid phenotype who would not develop psychosis.
While some individuals show relatively stable patterns of subtle social and neurocognitive impairments, those who develop schizophrenia typically enter a prodromal phase characterized by a gradual but marked decline in social and academic functioning which precedes the onset of active psychotic symptoms. An insidious deterioration prior to onset of psychosis is typical of the presentation of schizophrenia in children and adolescents (Werry et al. 1994). In the Maudsley study of adolescent psychoses (Hollis 1999) a pattern of insidious onset was found more often in cases of schizophrenia than in affective psychoses. Non-specific behavioural changes including social withdrawal, declining school performance, uncharacteristic and odd behaviour began, on average, over 1 year before the onset of positive psychotic symptoms. In retrospect, it was often apparent that non-specific behavioural changes were frequently early negative symptoms, which in turn had their onset well before positive symptoms such as hallucinations and delusions.
Hence, early recognition of disorder can be very difficult, as premorbid cognitive and social impairments gradually shade into prodromal symptoms before the onset of active psychotic symptoms (Hafner & Nowotny 1995). Prodromal symptoms can include odd ideas, eccentric interests, changes in affect, unusual experiences and bizarre perceptual experiences. While these are also characteristic features of schizotypal personality disorder, in a schizophrenic prodrome there is usually progression to more severe dysfunction.
Child and adolescent onset schizophrenia is characterized by more prominent negative symptoms (e.g. flattened or inappropriate affect and bizarre manneristic behaviour), disorganized behaviour, hallucinations in different modalities and relatively fewer well-formed systematized or persecutory delusions than adult schizophrenia (Garralda 1984; Asarnow & Ben-Meir 1988; Green et al. 1992; Werry et al. 1994). Taking the DSM-IIIR subtypes of schizophrenia, Beratis et al. (1994) found that the disorganized and undifferentiated subtypes were predominantly of adolescent onset while the paranoid subtype was most frequently first diagnosed in adult life. While all subtypes can occur in adolescence, there is a relative predominance of the disorganized subtype which in earlier systems of classification would have been described as hebephrenia.