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Our objective was to assess the validity of the Edinburgh Cognitive and Behaviour ALS Screen (ECAS), a multi-domain screen designed to detect cognitive deficits in patients with motor disorders. Forty ALS patients (without pre-diagnosed dementia) and 40, age-, gender- and education-matched healthy controls were recruited. All participants underwent extensive neuropsychological assessment and the ECAS. Performance at neuropsychological assessment across five domains (fluency, executive function, language, memory and visuospatial function) was compared to the ECAS ALS-Specific (fluency, executive functions and social cognition, language), ALS Non-specific (memory, visuospatial functions), and Total scores. Data from the healthy controls produced population-based abnormality cut-offs: composite score performance ≤ 2 SD in any domain classified impairment at neuropsychological assessment. Thirty-three percent of patients were impaired, most commonly in a single domain (executive or language dysfunction). Receiver Operator Curve (ROC) analyses using ECAS Total scores and ALS-Specific scores revealed 85% sensitivity and 85% specificity in the detection of cognitive impairment characteristic of ALS (fluency, executive function, language). A five-point borderline range produced optimal values (ALS-Specific Score 77-82, and ECAS-Total Score 105-110). In conclusion, validation against gold standard extensive neuropsychology demonstrated that the ECAS is a screening tool with high sensitivity and specificity to impairment characteristic of ALS.

Three experiments investigated younger (18-25 yrs) and older (70-88 yrs) adults' temporary memory for colour-shape combinations (binding). We focused upon estimating the magnitude of the binding cost for each age group across encoding time (Experiment 1; 900/1500 ms), presentation format (Experiment 2; simultaneous/sequential), and interference (Experiment 3; control/suffix) conditions. In Experiment 1, encoding time did not differentially influence binding in the two age groups. In Experiment 2, younger adults exhibited poorer binding performance with sequential relative to simultaneous presentation, and serial position analyses highlighted a particular age-related difficulty remembering the middle item of a series (for all memory conditions). Experiments 1-3 demonstrated small to medium binding effect sizes in older adults across all encoding conditions, with binding less accurate than shape memory. However, younger adults also displayed negative effects of binding (small to large) in two of the experiments. Even when older adults exhibited a greater suffix interference effect in Experiment 3, this was for all memory types, not just binding. We therefore conclude that there is no consistent evidence for a visual binding deficit in healthy older adults. This relative preservation contrasts with the specific and substantial deficits in visual feature binding found in several recent studies of Alzheimer's disease.

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Objective. Several studies have reported that people with Parkinson’s disease (PD) perform poorly on tests of ‘Theory of Mind’ (ToM), suggesting impairment in the ability to understand and infer other people’s thoughts and feelings. However, few studies have sought to separate the processes involved in social reasoning from those involved in managing the inhibitory demands on these tests. In this study, we investigated the contribution of inhibition to ToM performance in PD. Methods. 18 PD patients and 22 age-matched healthy controls performed a ToM test that separates the ability to infer someone else’s perspective from the ability to inhibit one’s own. Participants also completed a battery of standard measures of social and executive functioning, including measures of inhibition. Results. The PD patients performed worse on the ToM test only when the inhibitory demands were high. When the level of inhibition required was reduced, there were no significant group differences. Furthermore, executive impairments in PD patients were limited to measures of inhibition, with disadvantages associated with poorer ToM performance in this group. Conclusions. This study provides convincing evidence that the apparent impairment observed on ToM tests in PD is explained by deficits in inhibition.