Childhood Cognitive Functioning in Schizophrenia Patients and Their Unaffected Siblings: A Prospective Cohort Study

Abstract

While it is known that children of schizophrenia parents perform more poorly on tests of cognitive functioning than children of normal parents, less certain is the degree to which such deficits predict schizophrenia outcome, whether cognitive functioning deteriorates during childhood in preschizophrenia individuals, and whether nongenetic etiologic factors (such as obstetric complications) contribute to these deficits. In the present study, 72 patients with schizophrenia or schizoaffective disorder, 63 of their siblings not diagnosed with schizophrenia, and 7,941 controls with no diagnosis were ascertained from a birth cohort whose members had been evaluated with standardized tests of cognitive functioning at 4 and 7 years of age. Adult psychiatric morbidity was ascertained via a longitudinal treatment data base indexing regional public health service utilization, and diagnoses were made by review of all pertinent medical records according to DSAf-TV criteria. Both the patients with schizophrenia and their unaffected siblings performed significantly worse than the nonpsychiatric controls (but did not differ from each other) on verbal and nonverbal cognitive tests at 4 and 7 years of age. Preschizophrenia cases and their siblings were increasingly overrepresented across decreasing quartiles of the performance distributions. There was not significant intra-individual decline, and there were no significant relationships between obstetric complications and test performance among the preschizophrenia subjects. These results suggest that during the period from age 4 to age 7 years, premorbid cognitive dysfunction in schizophrenia represents a relatively stable indicator of vulnerability deriving from primarily genetic (and/or shared environmental) etiologic influences. Findings of cytoarchitectural and morphologic brain changes consistent with a prenatal and perinatal origin have led to the notion that neurodevelopmental disturbances contribute to the etiology of at least some cases of adult schizophrenia (Kovelman and Scheibel 1984;Jakob and Beckmann 1986;Weintraub 1987;Arnold et al. 1991;Akbarian et al. 1993;Cannon et al. 1993). However, the etiologic correlates of these disturbances and the proportion of the population with schizophrenia that they characterize remain to be determined (Lewis and Murray 1987;Cannon and Mednick 1991). Prospective examination of cognitive functioning in individuals who develop schizophrenia as adults provides an indirect means to address these questions. Longitudinal "high-risk" studies have consistently reported that children of patients with schizophrenia perform more poorly on neuropsychological tests than children of other people (Mednick and Schulsinger 1968;Landau et al. 1972;Asarnow et al. 1978;Rutschmann et al. 1980;Harvey et al. 1981;Winters et al. 1981;Worland et al. 1982;Driscoll 1984;Lifshitz et al. 1985;Sohlberg 1985;Hallett et al. 1986;Fish 1987;Goodman 1987;Sameroff et al. 1987;Weintraub 1987;Erlenmeyer-Kimling et al. 1989;Schreiber et al. 1992;Marcus et al. 1993...

Familial covariation of facial emotion recognition and IQ in schizophrenia

“…alterations in general intellectual ability and social cognition) seen in patients with schizophrenia are now recognized as a core feature of the disorder (Billeke and Aboitiz, 2013;Cannon et al, 2000;Elvevag and Goldberg, 2000). Not specific to the illness' subtypes, they are evident at the onset of the illness (in unmedicated patients), largely stateindependent and persistent in a trait-like fashion, thus potentially reflecting a genetic liability to schizophrenia-spectrum disorders.…”

“…alterations in general IQ and facial emotion recognition), it has been proposed that aforementioned cognitive changes might represent indicators of vulnerability to schizophrenia-spectrum disorders, deriving from primarily genetic (and/or shared environmental) etiologic influences (Cannon et al, 2000;Lavoie et al, 2013).…”

Catechol-O-methyl transferase Val158Met gene polymorphism in schizophrenia: working memory, frontal lobe MRI morphology and frontal cerebral blood flow

“…12 Schizophrenia patients as well as their unaffected relatives perform poorly on tasks that assess working memory function. [13][14][15][16][17][18][19][20][21][22][23] Working memory is moderately heritable with 43-49% of its variability accounted by genetic factors 24 In a series of studies involving a population isolate, a significant additive genetic heritability estimate was found in verbal working memory, and for visual working memory at a trend level. 20,21,25 Spatial working memory performance was more highly correlated in monozygotic twins than in dizygotic twin pairs.…”

Review paper. Neuropsychological dimension of schizophrenia - evaluation possibilities and therapeutic implications

“…Both numerous reports in the literature and clinical observations of patients with schizophrenia lead to the conclusion that cognitive impairment in most cases is preceded by the outbreak of psychosis [48,49,50,51,52]. Moreover, its severity in patients with the first episode of schizophrenia may be associated with the time elapsed since the onset of psychotic symptoms to undertaking of appropriate treatment [53].…”

“…Zarówno liczne doniesienia w literaturze, jak i obserwacje kliniczne osób chorych na schizofrenię pozwalają na stwierdzenie, że zaburzenia funkcji poznawczych w większości przypadków wyprzedzają wybuch psychozy [48,49,50,51,52] a ich nasilenie u osób z pierwszym epizodem schizofrenii może być związane z czasem, jaki upłynął od wystąpienia pierwszych objawów psychotycznych do podjęcia stosownego leczenia [53]. Tę niedomogę poznawczą, szczególnie w zakresie pamięci słownej, funkcji wykonawczych, pamięci operacyjnej i pamięci globalnej już w pierwszym epizodzie psychotycznym potwierdzają dane z badań Bildera [48].…”