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Studies of Parkinson's disease (PD) have shown impaired temporal ordering but interpretation may be confounded by task requirements and the effects of medication. We examined item recognition and recency discrimination in PD in relation to treatment and performance on other tests. Patients showed increased response latency and impaired recency discrimination only at short retention intervals. The deficits were greater in chronically medicated patients but treatment with levodopa, bromocriptine or anticholinergic drugs did not affect performance of newly diagnosed cases. The short-term memory deficits correlated with scores on tests of working memory, attention and executive function. These results do not indicate a generalised temporal ordering deficit in PD but suggest that much of the cognitive impairment in the disorder arises from attentional deficits affecting short-term and working memory.

The encoding ability of 17 amnesics of mixed aetiology and 17 matched normal controls was assessed directly using a novel procedure. On two separate occasions, subjects were shown 60 complex drawings each containing six pictures. On one occasion each drawing was shown for 6 sec, and on the other occasion it was shown for 25 sec. Immediately after presentation of each drawing subjects were asked a single unpredictable question about picture colours, location, size or semantic category. Amnesics performed normally in the 6-sec exposure condition indicating that all the tested kinds of information were encoded at a normal rate. Performance in this condition correlated with short-term, but not long-term memory in the amnesics indicating that it depended largely on encoding and short-term memory. However, the amnesics were impaired in the 25-sec condition where performance should have depended on (long-term) memory abilities at which they were impaired. The results are inconsistent with available encoding deficit accounts of amnesia.

This study investigated the possibility that the previously mixed findings relating to cognitive deficits in Parkinson's disease might be attributable to inhomogeneity within the patients sampled, with attentional deficits occurring only for those Parkinson's patients who also have additional frontal lobe impairment. Twenty-five patients with idiopathic Parkinson's disease were classified as showing frontal dysfunction, or not, on the basis of their performance on the Wisconsin Card Sorting Test and the picture arrangement subtest of the WAIS. The two groups, and a control group of normal elderly subjects matched for age and IQ, undertook tests of visual attention designed to dissociate baseline response speed from central information processing speed. Error rates did not differ between the groups. Performance of the non-frontally impaired Parkinson's group was indistinguishable from that of the controls. By contrast, the 'frontally impaired' Parkinson's group responded significantly more slowly than the controls. Further analyses indicated that for the frontally-impaired Parkinson's group, information processing and automatic functions were unimpaired but there was a generalised slowing (as reflected by increased baseline response time) which may represent a non-specific global cognitive impairment. These findings suggest that the frontal lobes may be implicated in slowed response speed in Parkinson's disease.

Stem-completion priming performance in patients with Alzheimer's type dementia (DAT) was explored in three experiments in which both the standard repetition priming effect and a novel indirect form of priming, cohort priming, were measured. In the first experiment, in which study stimuli were words, both priming effects were found to be markedly attenuated in the DAT group. In the second experiment, the study stimuli were specially constructed nonwords, and it was found that cohort priming was present at normal levels in the DAT group. In a third experiment we tested the specific hypothesis that the requirement to overtly articulate target stimuli during the study phase was critical for the appearance of normal cohort priming in the DAT group in Experiment 2, and also for the normal levels of repetition priming which have been reported in some published studies. Two encoding conditions were compared, one in which subjects simply had to read aloud the target words and a second in which subjects were required to make evaluative (pleasantness) ratings for each of the target words (identical to that used in Experiment 1). Stem-completion priming performance following the latter condition was significantly attenuated in the DAT group relative to a healthy control group, but following the "read aloud" encoding condition, normal levels of repetition and cohort priming were observed. It is suggested that the most fruitful approach to understanding the performance of DAT subjects on lexical repetition priming tasks will involve a detailed analysis of language functions and how they interact with other, possibly mnemonic, processes in the generation of primed responses.

The relationship of release from proactive interference (PI) to set-shifting, explicit free recall and language remains controversial. We tested 56 patients with Parkinson's disease (PD) who had never received medication and 37 matched normal control subjects on a test of PI release based on semantic category. The PD group showed normal PI release but impaired word recall. PI release was independent of impaired Wisconsin card-sorting test performance, language production, explicit memory, overall cognitive status and severity of depression. The results indicate dissociation between ability to benefit from semantic stimulus properties and processes of explicit memory, set-shifting and expressive language.