Etiological heterogeneity and intelligence test scores in patients with schizophrenia.

Previous research has indicated that patients with a family history of schizophrenia show a greater degree of cognitive and neuropsychological impairment than patients without a family history. We examined the neurocognitive performance, using the WAIS-R, of 51 patients with a family history (familial) and 103 patients without a family history (sporadic) to determine if differences exist that may help to explain the heterogeneous neuropsychological profile of the illness. The family history groups did not differ with respect to gender, diagnosis, ethnicity, age, age of onset, education or duration of illness. Multivariate analyses, covarying for age of onset and education, showed the sporadic group performed significantly better than the familial group on the digit symbol and object assembly subtests, with a trend level difference in overall performance IQ score. Additionally, we identified significant gender differences in favor of males for full scale and verbal IQ, the information, digit span, block design, and arithmetic subtests, and at a trend level, the picture assembly subtest. The family history group differences reflect relative dysfunction in visual attention and scanning, visuomotor control, and spatial processing and reasoning. Overall, the results suggest that sporadic patients have better perceptual-organizational skills and faster speed of processing.

Paternal age and intelligence: implications for age-related genomic changes in male germ cells.

BACKGROUND: A robust association between advancing paternal age and schizophrenia risk is reported, and genetic changes in the germ cells of older men are presumed to underlie the effect. If that is so, then the pathway may include effects on cognition, as those with premorbid schizophrenia are reported to have lower intelligence. There are also substantial genetic influences on intelligence, so de novo genetic events in male germ cells, which accompany advancing paternal age, may plausibly influence offspring intelligence. OBJECTIVE: An association of paternal age with IQ in healthy adolescents may illuminate the mechanisms that link it to schizophrenia. METHOD: We examined the association of paternal age and IQ scores using the Israeli Army Board data on 44 175 individuals from a richly described birth cohort, along with maternal age and other potential modifiers. RESULTS: A significant inverted U-shaped relationship was observed between paternal age and IQ scores, which was independent from a similar association of IQ scores with maternal age. These relationships were not significantly attenuated by controlling for multiple possible confounding factors, including the other parent's age, parental education, social class, sex and birth order, birth weight and birth complications. Overall, parental age accounted for approximately 2% of the total variance in IQ scores, with later paternal age lowering non-verbal IQ scores more than verbal IQ scores. CONCLUSION: We found independent effects of maternal and paternal age on offspring IQ scores. The paternal age effect may be explained by de novo mutations or abnormal methylation of paternally imprinted genes, whereas maternal age may affect fetal neurodevelopment through age-related alterations in the in-utero environment. The influence of late paternal age to modify non-verbal IQ may be related to the pathways that increase the risk for schizophrenia in the offspring of older fathers.

The reliability and clinical correlates of figure-ground perception in schizophrenia.

Schizophrenia subjects are impaired in a number of visual attention paradigms. However, their performance on tests of figure-ground visual perception (FGP), which requires subjects to visually discriminate figures embedded in a rival background, is relatively unstudied. We examined FGP in 63 schizophrenia patients and 27 control subjects and found that the patients performed the FGP test reliably and had significantly lower FGP scores than the control subjects. Figure-ground visual perception was significantly correlated with other neuropsychological test scores and was inversely related to negative symptoms. It was unrelated to antipsychotic medication treatment. Figure-ground visual perception depends on "top down" processing of visual stimuli, and thus this data suggests that dysfunction in the higher-level pathways that modulate visual perceptual processes may also be related to a core defect in schizophrenia.

Trail making and olfaction in schizophrenia: implications for processing speed.

BACKGROUND: Previous research has established a relationship between smell identification deficits (SID) and particular aspects of cognitive function among patients with schizophrenia. OBJECTIVE: To expand the extant literature, we examined the relationship between SID and the Trail Making Test to determine if processing speed is related to SID. METHODS: Our sample included 60 inpatients from the New York State Psychiatric Institute's Schizophrenia Research Unit. We considered age, deficit syndrome, verbal intelligence quotient, and education in our analyses due to their documented relationship to smell identification ability. RESULTS: Trails A errors and Trails A seconds accounted for a significant amount of the variance in University of Pennsylvania Smell Identification Test scores in a regression analysis (R2=.10, P=.008 and R2=.05, P=.04). CONCLUSION: Linking neurocognition to smell identification deficits may prove to be an essential marker for schizophrenia research.

A brief smell identification test discriminates between deficit and non-deficit schizophrenia.

Evidence is accumulating that smell identification deficits (SID) and social dysfunction in schizophrenia may share a common pathophysiology. While most schizophrenia studies utilize the lengthy 40-item University of Pennsylvania Smell Identification Test (UPSIT) to assess smell identification ability, a brief 12-item smell identification test (B-SIT) has recently been constructed as a culturally neutral substitute for the UPSIT. By selecting the 12 items of the UPSIT from which the B-SIT was originally derived, we constructed a proxy for the B-SIT and compared the performance of 83 patients with schizophrenia to 69 normal subjects. We examined select properties of the B-SIT proxy in relation to the UPSIT to determine its efficacy for use in psychiatric populations. We considered the sensitivity of the B-SIT proxy and evaluated a cutoff score for identifying deficit syndrome schizophrenia (DS). The UPSIT and B-SIT proxy were significantly related in the patients (n=83, r=0.85, P=0.01) and in comparison subjects (n=69, r=0.83, P=0.01), and both measures similarly distinguished DS from non-deficit syndrome (non-DS) patients. The results of this study support the utility of the B-SIT for schizophrenia research and highlight the robustness of the relationship between SID and social dysfunction in schizophrenia.