Richard Cosway

Neuropsychological change in young people at high risk for schizophrenia: results from the first two neuropsychological assessments of the Edinburgh High Risk Study.

BACKGROUND Studies of groups of individuals who have a genetically high risk of developing schizophrenia, have found neuropsychological impairments that highlight likely trait markers of the schizophrenic genotype. This paper describes the change in neuropsychological function and associations with psychiatric state of high risk participants during the first two assessments of the Edinburgh High Risk Study. METHODS Seventy-eight high risk participants and 22 normal controls, age and sex matched completed two neuropsychological assessments 18 months to 2 years apart. The areas of function assessed include intellectual function, executive function, learning and memory, and verbal ability and language. RESULTS The high risk participants performed significantly worse on particular tests of verbal memory and executive function over the two assessments than matched controls. Those high risk participants who experienced psychotic symptoms were found to exhibit a decline in IQ and perform worse on tests of verbal memory and executive function than those without symptoms. An increase in psychotic symptoms between the two assessments in the high risk group was found to be associated with an apparent decline in IQ and memory. CONCLUSIONS The results suggest that the development of psychotic symptoms is preceded by a decline in IQ and memory. This may reflect a general and a more specific disease process respectively.

Neuropsychology, Genetic Liability, and Psychotic Symptoms in Those at High Risk of Schizophrenia

Neuropsychological assessments were compared among individuals at enhanced genetic risk of schizophrenia (n = 157) and controls (n = 34). The relationship between cognitive impairments and the presence of psychotic symptoms and measures of genetic risk was explored in the high-risk subjects. Neuropsychological differences were identified in many areas of function and were not accounted for by the presence of psychotic symptoms. Genetic liability was not associated with neuropsychological performance or with psychotic symptoms, but exploratory analysis showed some tests were associated with both liability measures. These results suggest that what is inherited is not the disorder itself but a state of vulnerability manifested by neuropsychological impairment, occurring in many more individuals than are predicted to develop the disorder.

The effect of sleep fragmentation on cognitive processing using computerized topographic brain mapping

Topographic brain mapping of evoked potentials can be used to localize abnormalities of cortical function. We evaluated the effect of sleep fragmentation on brain function by measuring the visual P300 waveform using brain mapping. Eight normal subjects (Epworth Score ± SD: 5 ± 3) underwent tone‐induced sleep fragmentation and undisturbed study nights in a randomized cross‐over design. Study nights were followed by topographic brain mapping using a visual information processing test and concurrent event‐related potentials. Experimental sleep fragmentation did not significantly increase objective daytime sleepiness or lower cognitive performance on a battery of cognitive function tests (all P ≥ 0.1). There were no significant topographical delays in P300 latencies with sleep fragmentation (all P > 0.15). However, at sites Fz, F4, T3, C3, Cz and C4 the P300 amplitudes were reduced significantly after sleep fragmentation (all P < 0.05). A reduction in P300 amplitude has previously been interpreted as a decrease in attention. These reductions in P300 amplitudes with sleep fragmentation in frontal, central and temporal brain areas suggest that sleep fragmentation may cause a broad decrease in attention. Sleep fragmentation did not delay P300 latencies in any brain area, and so does not explain the delay in P300 latencies reported in sleep apnoeics.

Measurement of lateral preferences and schizophrenia: results of the Edinburgh High-Risk Study and methodological issues

The assessment and measurement of handedness has varied across studies, limiting the comparability of results. Data from the Edinburgh High Risk for Schizophrenia Study were analyzed to investigate the effect of different methods of assessment and scoring of hand preferences on the prevalence of handedness type and on between-group differences in handedness. Handedness was measured using both the Edinburgh Handedness Inventory and the Annett Handedness Scale in 143 subjects at high risk for schizophrenia, 31 control subjects, and 27 patients with a first episode of schizophrenia. Hand preferences were identified through demonstration of items and by verbal report. No group differences were found, although the prevalence of hand preferences changed substantially depending on the definition used. Significant correlations with socio-demographic factors were found in some instances, but these correlations depended on the definition of handedness. No sex differences were identified. The magnitude of group differences remained similar, although the prevalence of handedness types varied greatly with changes in definition of handedness. Care should be taken in correlation studies to avoid spurious relationships between handedness and other factors. To allow for comparability of results across studies, researchers should adopt a standard definition of handedness.