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S Corkin

Publications and source records attributed to S Corkin.

At least 37 records · Page 2Linked to original sources
PubMed1997

The time course of spatial and object learning in Parkinson's disease.

Parkinson's disease (PD) is characterized by spatial memory dysfunction, but the selectivity of the deficit remains unclear. We addressed this issue by comparing performance on spatial and object variants of a conditional associative learning task, and by analysing the data with time series analytical techniques. The 11 PD subjects and 15 normal control subjects learned stimulus-stimulus pairings through trial-and-error learning. PD subjects were selectively impaired on the spatial condition: they required more trials to achieve criterion, learned at a slower rate and displayed a working memory deficit. The groups did not differ in the object condition. These results suggest a distinction between material-specific spatial and object visual memory systems. Further, they indicate that spatial learning and memory are selectively impaired in early PD, suggesting that interactions between the basal ganglia and prefrontal cortex are important for the mediation of high-level cognition.

Aged↗
PubMed1997

Spatial, but not object, delayed response is impaired in early Parkinson's disease.

The authors hypothesized that the pathophysiology of early Parkinson's disease (PD) may selectively target structures that support visual working memory for spatial relations but leave structures that support working memory for featural characteristics of objects relatively intact. Fifteen PD and 15 normal control participants took a visual delayed-response test with a spatial condition and a (nonspatial) object condition, equating the perceptual difficulty of the tests for each participant. The stimuli were irregular polygons presented at different locations on a computer screen. Results revealed a selective impairment of spatial delayed response in PD, indicating a disruption of spatial working memory unconfounded by sensory processing difficulties. The selectivity of this deficit may reflect the circumscribed nature of pathophysiological change affecting the caudate nucleus in early PD.

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PubMed1996

The hippocampal formation participates in novel picture encoding: evidence from functional magnetic resonance imaging.

Considerable evidence exists to support the hypothesis that the hippocampus and related medial temporal lobe structures are crucial for the encoding and storage of information in long-term memory. Few human imaging studies, however, have successfully shown signal intensity changes in these areas during encoding or retrieval. Using functional magnetic resonance imaging (fMRI), we studied normal human subjects while they performed a novel picture encoding task. High-speed echo-planar imaging techniques evaluated fMRI signal changes throughout the brain. During the encoding of novel pictures, statistically significant increases in fMRI signal were observed bilaterally in the posterior hippocampal formation and parahippocampal gyrus and in the lingual and fusiform gyri. To our knowledge, this experiment is the first fMRI study to show robust signal changes in the human hippocampal region. It also provides evidence that the encoding of novel, complex pictures depends upon an interaction between ventral cortical regions, specialized for object vision, and the hippocampal formation and parahippocampal gyrus, specialized for long-term memory.

Adult↗
PubMed1996

Apolipoprotein E genotype does not influence rates of cognitive decline in Alzheimer's disease.

BACKGROUND: Inheritance of the apolipoprotein E (apoE) epsilon 4 allele is a risk factor for developing Alzheimer's disease (AD) and is associated with a lower age of dementia onset. The purpose of this study was to determine whether apoE genotypes differentially influence the course of cognitive decline in AD dementia. METHODS: We administered nine cognitive tests that assessed explicit memory, attention, language, visuospatial function, frontal-lobe function, and logical reasoning abilities to 66 probable AD patients every 6 to 24 months over a span of up to 5.5 years. We identified apoE genotype by a PCR-based method; there were 16 patients with epsilon 3/3, 34 with epsilon 3/4, and 16 with epsilon 4/4. Using regression statistical methods, we computed the change in performance for each test for each patient over time. We then analyzed the mean change in each test in patients grouped according to apoE genotype. RESULTS: For the AD patients as a group, performance on all cognitive tests declined significantly over time, but the rate of decline did not vary significantly across apoE genotypes on any cognitive test. Specifically, the rate of cognitive decline was not faster in patients with an epsilon 4 allele than in those with epsilon 3/3. CONCLUSIONS: These results indicate that the mechanism placing individuals with an epsilon 4 allele at risk for developing AD does not influence the rate of cognitive decline. These observations imply that the influence of apoE epsilon 4 either precedes or occurs at an early point in the AD disease process.

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PubMed1995

Cognitive test performance in detecting, staging, and tracking Alzheimer's disease.

OBJECTIVES: To identify the specific cognitive deficits that characterize Alzheimer's disease (AD) and determine which cognitive tests, or combination of tests, are best for detecting AD (ie, distinguishing patients with AD from normal control subjects), staging AD (ie, distinguishing different severities of dementia), and tracking disease progression. SUBJECTS: Patients with AD (n = 123) and normal control subjects (n = 60) of comparable age, education, and gender distribution. SETTING: Outpatient care. MEASURES: Ten cognitive tests of memory, language, visuospatial abilities, and reasoning; the Information, Memory and Concentration subtest of the Blessed Dementia Scale, and the total score on an activities of daily living questionnaire. DESIGN: Patients with AD were tested every 6 to 24 months over a span of up to 5.5 years. RESULTS: Patients with AD were significantly inferior to normal control subjects on all cognitive tests. The scores of patients with AD worsened over time. Delayed recall of stories and figures showed sharp deterioration to an early floor, consistent with the finding that these tests discriminated patients with mild AD from normal control subjects well but were poor for staging. Confrontation naming, semantic fluency, and immediate recognition of geometric figures showed steady linear decline across time for patients with AD, consistent with these tests being found best for staging dementia severity. CONCLUSIONS: We postulate that the pathologic bases of impairment in delayed recall are atrophy of cholinergic ventral forebrain neurons and partial deafferentation of the hippocampus, both of which occur early in the course of AD. Worsening language and visuospatial abilities likely reflect progressive loss of neocortical neurons and their connections.

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PubMed1995

Double dissociation of memory capacities after bilateral occipital-lobe or medial temporal-lobe lesions.

Memory for recently encountered information can be reflected in conscious recall and recognition of that material, or in facilitated reprocessing of that material, an effect known as repetition priming. Repetition priming may be perceptual (form-based) or conceptual (meaning-based). A patient with bilateral occipital-lobe lesions (L.H.) and a patient with bilateral medial-temporal lobe lesions (H.M.) showed a double dissociation between visuoperceptual priming (impaired in L.H. and intact in H.M.) and visual recognition memory (intact in L.H. and impaired in H.M.). L.H. showed intact conceptual priming for visually presented words; his pattern of impaired visuoperceptual priming and intact conceptual priming is the reverse dissociation to that observed in prior studies of patients with Alzheimer's disease, in whom occipital cortices are relatively spared. These double dissociations suggest that a memory system localized to the occipital lobe mediates visuoperceptual priming effects, and that this system is independent of neural circuits mediating conceptual priming effects, and independent of the limbic-diencephalic system supporting conscious recognition of recently encountered information.

Adult↗
PubMed1995

Prevalence of visual deficits in Alzheimer's disease.

This study addressed the issue of prevalence and pattern of visual deficits in 77 subjects with Alzheimer's disease (AD) and 111 healthy control subjects. We defined cutoff scores that would be expected from only 1 control subject of 100 (p = 0.01). The percentage of AD subjects who performed at or worse than this level varied across the 16 visual tests from a high of 58% to a low of 0%. The distribution of impairment across tests suggests a high vulnerability in AD of pattern vision, moderate vulnerability of spatial vision, and low vulnerability of motion and flicker perception. We found evidence for heterogeneity in the AD subject group: a subgroup (N = 14) emerged that was characterized by poor performance on the Backward Pattern Masking test, relatively young age, and relatively short duration of AD. Overall, the results indicate that visual dysfunction, especially on Backward Masking, is a common sign of AD.

Aged↗
PubMed1995

Visual dysfunction predicts cognitive deficits in Alzheimer's disease.

Deficits in basic visual capacities are prevalent in Alzheimer's disease (AD), raising the question of their impact on cognitive function. We examined the relation between vision and cognition in 72 patients with AD. Vision tests assessed color discrimination, stereoacuity, contrast sensitivity, and backward pattern masking. For cognitive tests of object recognition, at least 25% (up to 50%) of score variance was predicted by performance on a vision test. For tests of spatial localization, only 2 to 11% of the variance was predicted by performance on a vision test. The results indicated that: (1) visual dysfunction was a significant predictor of cognitive dysfunction in AD, and (2) visual deficits in AD may have a strong functional impact on performance in specific cognitive domains.

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PubMed1994

Priming in perceptual identification of pseudowords is normal in Alzheimer's disease.

Patients with Alzheimer's disease (AD) have deficits in recall and recognition memory, and show dissociable performance in repetition priming tasks: They exhibit impaired priming in word-completion and word-generation tasks, but normal priming is perceptual identification of words. In order to examine whether AD patients can show normal priming with novel, unfamiliar stimuli, the present study examined their performance in perceptual identification of pseudowords. Despite impaired recognition memory performance, AD patients showed normal priming in perceptual identification of pseudowords. These results extend the boundaries of intact repetition priming in AD, demonstrating that such priming is not limited to stimuli that are pre-morbidly represented in long-term knowledge. Preserved repetition priming in AD may reflect the operation of perceptual processes localized to posterior visual circuits that are relatively spared in AD.

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PubMed1994

Impaired problem solving in Parkinson's disease: impact of a set-shifting deficit.

Parkinson's disease (PD) is associated with specific cognitive deficits in the absence of dementia, including the inability to suppress previously learned responses in a changed context. Our goal was to determine whether this set-shifting deficit is sufficient to account for impaired performance on a problem-solving task, or, instead, whether it is necessary to postulate deficits in one or more other cognitive capacities, such as logical deduction. Deductive reasoning and other conceptual abilities were assessed in 15 nondemented subjects with PD who had never been medicated, 15 nondemented subjects with PD who were currently receiving medication, and 15 healthy elderly control subjects. On a deductive reasoning task, Poisoned Food Problems, the PD groups made more errors than the control group. The PD groups' error pattern was characterized by intrusions of information from previous problems. By contrast, the PD groups made appropriate assessments of redundant and irrelevant information that appeared in these problems, and performed normally on other tests of concept formation and problem solving that did not require set shifting, indicating that the capacities for logical deduction and concept formation were intact. The set-shifting deficit, conceptualized as a difficulty in suppressing a prepotent response, appears to be a primary cognitive impairment in PD and presumably arises from dysfunction of the nigrostriatal-dorsolateral prefrontal cortex complex loop.

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PubMed1994

Dissociations among structural-perceptual, lexical-semantic, and event-fact memory systems in Alzheimer, amnesic, and normal subjects.

Patients with Alzheimer's disease (AD), patients with global amnesia (AMN), and normal control (NC) subjects received tests of recall and recognition, word-completion priming, and incomplete-picture priming. The AD and AMN patients had impaired recall and recognition. The AD patients, but not the AMN patients, had impaired word-completion priming. In contrast, the AD patients had intact incomplete-picture priming, a form of priming shown to be perceptual in normal subjects. These results provide neuropsychological evidence for a dissociation between two components of repetition priming, perceptual priming as measured with identification tasks and nonperceptual priming as measured with generation tasks. Preserved perceptual priming in AD may be mediated by the occipital regions that are relatively spared in AD; compromised nonperceptual priming may be mediated by temporal regions that show dense neuropathological changes early in AD.

Adult↗
PubMed1993

Intact acquisition and long-term retention of mirror-tracing skill in Alzheimer's disease and in global amnesia.

The ability of patients with Alzheimer's disease (AD) or global amnesia (AMN) to acquire skill for tracing a pattern seen in mirror-reversed view and to retain that skill over 24-h intervals was examined. Both patient groups had poor recall and recognition of their mirror-tracing experience, but they acquired and retained mirror-tracing skill as well as normal control subjects. One AMN patient (H.M.) retained the skill over a year-long interval. Furthermore, the patients transferred their skill normally to an alternate pattern. These results indicate that the memory system underlying mirror-tracing skill learning is separable from medial-temporal structures compromised in AMN and AD and from neocortical areas compromised in AD. Brain regions relatively spared in early AD, such as the basal ganglia or cerebellum, may mediate critical aspects of the learning of novel sensorimotor associations that underlie skilled mirror tracing.

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PubMed1993

Auditory function in Alzheimer's disease.

The pattern of cerebral degeneration in Alzheimer's disease (AD) patients suggests that basic auditory capacities should be normal in AD, whereas progressively higher levels of auditory function should be increasingly impaired. To test this hypothesis, we administered tests of auditory capacities associated with primary auditory cortex (sound localization and perception of complex tones) and auditory association cortex (phoneme discrimination, timbre discrimination, and tonal memory) to 19 mildly to moderately demented AD patients, 21 elderly control subjects (ECS), and 14 young control subjects (YCS). The results showed significant differences between YCS and ECS on phoneme discrimination with synthetic speech and on tonal memory. The AD group differed from the ECS group on sound localization, one measure of synthetic speech discrimination, and timbre discrimination. Performance did not correlate with age, dementia severity, or duration of illness on any test condition. These findings indicate that although AD is accompanied by specific auditory deficits, the increase in neuropathologic change between primary auditory and auditory association cortices is not reflected in an increased impairment of functions that are mediated by these areas. Degraded aural language comprehension, which is characteristic of AD, likely reflects disruption of language processes, rather than dysfunction specific to auditory circuits.

Acoustic Stimulation↗
PubMed1992

Retinocalcarine function in Alzheimer's disease. A clinical and electrophysiological study.

Impaired visual function in Alzheimer's disease (AD) could result from either precortical or cortical lesions, or both. In a parallel psychophysical study of visual function in AD, we found that contrast sensitivity function, color vision, stereoacuity, and backward masking were impaired relative to the performance of age-matched control subjects, whereas performance on a critical flicker fusion test was normal. The intent of the present study was to determine whether abnormalities of the retinocalcarine pathway contribute to visual dysfunction. We performed neuro-ophthalmological examinations on 38 patients with AD; from this group, 25 received additional psychophysical testing and 13 underwent electrophysiological testing. Clinical neuro-ophthalmological examinations, full-field electroretinograms, focal electroretinograms, and pattern visual evoked potentials were normal in all patients tested. There was no evidence of retinocalcarine abnormality specific to AD. We conclude that the visual impairment experienced by some patients with AD primarily results from involvement of the visual association cortices rather than from precortical damage, at least before the end stage of the disease.

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PubMed1992

Category knowledge in Alzheimer's disease: normal organization and a general retrieval deficit.

Three hypotheses that could account for deficits in the retrieval of category information in Alzheimer's disease (AD) were evaluated: abnormal organization, class- or category-specific vulnerability, and limitation by general factors, such as decreased processing speed. Relative to 18 elderly control subjects, 18 patients with AD produced fewer items in a category fluency task and had longer reaction times in a category decision task. The pattern of performance across categories on both tasks was normal in the AD group: The same categories elicited the most (or fastest) responses in both the control group and the AD group. AD patients showed normal performance in ranking of category exemplars by typicality. There was no evidence for differential accessibility by category or by class of information (animate vs. inanimate). The authors conclude that a general factor or factors limit(s) retrievability equally across all categories.

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PubMed1991

Visual dysfunction in Alzheimer's disease: relation to normal aging.

In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). Critical flicker fusion thresholds were normal, relative to age-matched healthy subjects. For color, the majority of the errors were tritanomalous (blue axis). Color and stereoacuity deficits were unrelated to severity of dementia, in accordance with models of vision that describe these functions as modular rather than diffuse for cortical localization. Although contrast sensitivity was depressed throughout the frequency range in AD, more patients were impaired at low than at high spatial frequencies, contrasting with the observed normal aging pattern of high-frequency loss. Healthy elderly subjects showed depressed critical flicker fusion thresholds and reduced contrast sensitivity at high frequencies, relative to the young group; differences between these groups were not found for the other vision tests. A subset of the AD group received detailed neuro-ophthalmological examination, and no abnormalities were found. This finding, taken together with normal thresholds for critical flicker fusion, suggests that the widespread visual dysfunction reported here is more likely to be related to known pathological changes in primary visual and association cortex in AD than to changes in the retina or optic nerve.

Adolescent↗
PubMed1991

Evidence for a dissociation between perceptual and conceptual priming in Alzheimer's disease.

The status of perceptual priming and word-completion priming in patients with Alzheimer's disease (AD) was examined. Experiment 1 established the reliability of the perceptual priming measure in normal subjects. In Experiment 2, AD patients showed a normal magnitude of perceptual priming. In Experiment 3, a single group of AD patients showed a normal magnitude of perceptual priming and impaired word-completion priming. Further, word-completion priming, but not perceptual priming, was correlated with verbal fluency performance in AD. These results suggest a dissociation between two components of verbal priming. Perceptual priming may reflect the operation of a structural-perceptual memory system mediated by occipital lobe regions relatively spared in AD. Word-completion priming may reflect the operation of a lexical-semantic memory system mediated by temporoparietal lobe regions compromised in AD.

Adult↗