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B Deweer

Publications and source records attributed to B Deweer.

At least 37 records · Page 2Linked to original sources
PubMed1995

The neuropsychological pattern of corticobasal degeneration: comparison with progressive supranuclear palsy and Alzheimer's disease.

The pattern of cortical and subcortical neuropathologic lesions in corticobasal degeneration (CBD) should predict a specific cognitive profile in this disease. To characterize this profile and to determine its specificity by comparison with progressive supranuclear palsy (PSP) and senile dementia of the Alzheimer's type (SDAT), we used an extensive neuropsychological battery assessing global efficiency, executive functions, various tests of encoding and retrieval, dynamic motor organization, and upper limb praxis. We compared the performance of patients with CBD (n = 15) with that of controls (n = 19) matched for age and education, and with that of patients with PSP and SDAT (15 in each group), matched for severity of dementia and depression. Patients with CBD showed: (1) a moderate global deterioration; (2) a dysexecutive syndrome similar to that of patients with PSP and more severe than in SDAT; (3) explicit learning deficits, without retention difficulties and easily compensated by using the same semantic cues at encoding and retrieval as in PSP; this was in contrast with SDAT where cued recall and recognition were also impaired; (4) disorders of dynamic motor execution (temporal organization, bimanual coordination, control, and inhibition) similar to those of patients with PSP and not in SDAT; (5) asymmetric praxis disorders (posture imitation, symbolic gesture execution, and object utilization) that were not observed in PSP or SDAT. Patients with CBD show a specific neuropsychological pattern associating a dysexecutive syndrome, likely due to degeneration of the basal ganglia and prefrontal cortex, and asymmetric praxis disorders, which might be related to premotor and parietal lobe lesions. This neuropsychological profile may help to distinguish this condition clinically from other neurodegenerative diseases.

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PubMed1994

Explicit memory, procedural learning and lexical priming in Alzheimer's disease.

Different aspects of memory functions were studied in two groups of patients with Alzheimer's disease (AD) and in normal elderly controls. The tests included: explicit memory tests with free and cued recall, and recognition measures; learning of a motor skill; learning of a perceptual skill with verbal material; a priming task with the word stem completion paradigm. The data confirmed that, besides severe impairment for all measures of explicit memory, AD patients were able to learn and retain normally a motor skill in the rotor pursuit task, even across a long retention interval. Moreover, sparing of procedural learning was not restricted to motor tasks, since patients learned normally a mirror-reading task, demonstrating (a) rapid acquisition of the procedure, and (b) acquisition of item-specific information for repeated words. This last effect is accounted for in terms of repetition priming effects rather than of explicit memory strategies, since patients had also normal repetition effect in the word stem completion paradigm.

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PubMed1994

Relation of anosognosia to frontal lobe dysfunction in Alzheimer's disease.

A self-rating scale of memory functions was administered to 24 non-depressed patients with probable Alzheimer's disease, divided into two groups according to the overall severity of dementia (mild, mini-mental state (MMS) > 21; moderate, MMS between 10 and 20). These groups did not significantly differ in their self-rating of memory functions. The same questionnaire was submitted to a member of each patient's family, who had to rate the patient's memory. An "anosognosia score" was defined as the difference between patient's and family's ratings. This score was highly variable, and covered, in the two groups, the full range between complete awareness of deficits and total anosognosia. Correlations between the anosognosia score and several neuropsychological data were searched for. No significant correlation was found with either the Wechsler memory scale, the MMS, or linguistic abilities and gestures. In contrast, this score was highly correlated with the "frontal score", defined as the sum of scores on the Wisconsin card sorting test (WCST), verbal fluency, Luria's graphic series, and "frontal behaviours" (prehension, utilisation, imitation behaviours, inertia, indifference). Among these tests of executive functions, the highest correlation with the anosognosia score was obtained on the WCST. This suggests that anosognosia in Alzheimer's disease is not related to the degree of cognitive deterioration but results, at least in part, from frontal dysfunction.

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PubMed1994

Are explicit memory disorders of progressive supranuclear palsy related to damage to striatofrontal circuits? Comparison with Alzheimer's, Parkinson's, and Huntington's diseases.

To test the hypothesis that memory disorders of subcortico-frontal dementia result mainly from inefficiency of retrieval processes of stored information, we compared verbal learning in 15 patients with progressive supranuclear palsy, prototypical of "subcortical dementia," in free (California Verbal Learning Test) and controlled (Grober and Buschke's Test) encoding situations, with that of 19 controls, matched for age and level of education. The progressive supranuclear palsy patients showed memory deficits characterized by impaired immediate memory span, disturbed learning and consistency of recall, and abnormal number of false alarms at recognition, which were dramatically alleviated by controlled encoding associated with cued recall, using the same semantic cues. This memory profile was markedly different from that of patients with senile dementia of the Alzheimer type (n = 15), characterized by more rapid forgetting and less improvement in the controlled situation. Instead, it was similar to the memory pattern of patients with Parkinson's (n = 15) and Huntington's (n = 15) diseases. These results show a similar profile of memory disturbance in disorders involving damage to the striatofrontal system and suggest that the cortical and hippocampal lesions of PSP patients are insufficiently severe to interfere with the specific memory profile characteristic of the disease.

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PubMed1994

[Cognitive functions and the basal ganglia: the model of Parkinson disease].

Cognitive changes have long been observed in patients with degenerative diseases or focal lesions that involve primarily subcortical structures. Generally speaking, the deficits that have been reported in these diseases are similar and include: slowing of central processing; defective use of memory stores; impaired behavioural regulation in sorting tasks; disorders of plaining in tower-related tasks; and impaired manipulation of internal representation of visuo-spatial stimuli. Given the modulatory role of the basal ganglia and related structures, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well-defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.

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PubMed1994

Amygdalohippocampal MR volume measurements in the early stages of Alzheimer disease.

PURPOSE: To evaluate the accuracy of hippocampal and amygdala volume measurements in diagnosing patients in the early stages of Alzheimer disease. METHODS: Measurements of the hippocampal formation, amygdala, amygdalohippocampal complex (the two measurements summed), caudate nucleus, and ventricles, normalized for total intracranial volume, were obtained on coronal sections (1.5 T, 400/13 [repetition time/echo time], 5 mm) of 13 patients in the mild (minimental status > or = 21) and five patients in the moderate stages of Alzheimer disease (10 < minimental status < 21), and eight age-matched control subjects. RESULTS: For patients with a minimental status score of 21 or greater, atrophy was significant for the amygdala and hippocampal formation (-36% and -25% for amygdala/total intracranial volume and hippocampal formation/total intracranial volume, respectively), but not for the caudate nucleus. No significant ventricular enlargement was found. For patients with a minimental status score less than 21, atrophy was more severe in all structures studied (amygdala/total intracranial volume, -40%; hippocampal formation/total intracranial volume, -45%; caudate nucleus/total intracranial volume, -21%), and ventricles were enlarged (63%). No overlap was found between Alzheimer disease and control values for the amygdalohippocampal volume, even in the mild stages of the disease. In Alzheimer disease patients, hippocampal formation volumes correlated with the minimental status. CONCLUSION: Hippocampal and amygdala atrophy is marked and significant in the mild stages of Alzheimer disease. Volumetric measurements of the amygdala and the amygdalohippocampal complex appear more accurate than those of the hippocampal formation alone in distinguishing patients with Alzheimer disease.

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PubMed1993

Explicit memory in Alzheimer's, Huntington's, and Parkinson's diseases.

OBJECTIVE--Comparing the pattern of spared and impaired memory functions in neurodegenerative diseases known to affect different brain structures. DESIGN--Various situations of acquisition (free encoding or controlled encoding) and retrieval (immediate and delayed free and cued recall, recognition) were used. SETTING--Referral center. PATIENTS--Fifteen for each disease (ie, senile dementia of the Alzheimer type [SDAT], Parkinson's and Huntington's), matched for education, severity of dementia, and depression. MAIN OUTCOME MEASURES--Comparison of free and controlled encoding situations, relationships between memory, executive, and linguistic functions test scores. RESULTS--In the free encoding situation: no difference among the three groups, but higher numbers of intrusions and false recognitions in SDAT. In the controlled situation: cued recall and recognition scores significantly higher in Parkinson's disease and Huntington's disease than in SDAT. Memory performances correlated with executive functions test scores in Huntington's disease and Parkinson's disease, but not in SDAT. All results significant at P < .01. CONCLUSIONS--Clear distinction between the true amnesic syndrome of SDAT, compatible with lesions of hippocampus and temporal cortex, and the inefficient planning of memory processes of Huntington's disease and Parkinson's disease, which might result from a striatofrontal dysfunction.

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PubMed1993

Mirror reading in Alzheimer's disease: normal skill learning and acquisition of item-specific information.

Alzheimer's disease (AD) is characterized by severe explicit memory deficits and sparing of procedural learning. Most studies of skill learning in AD have been restricted to motor skills. This experiment was aimed at extending these studies to the domain of perceptual-verbal skills. Thirteen AD patients and 9 normal elderly controls were administered several explicit memory tests and a mirror reading paradigm with both unique and repeated word triads. In this last task, AD patients showed normal learning for unique word triads, that is, normal acquisition of the skill. Moreover, they benefitted from repeated triads to the same extent as did normal controls, although they were impaired in discriminating these repeated words from distractors at later recognition. These data demonstrate that patients with AD: (a) are able to learn and retain a perceptual-verbal skill at a normal rate; (b) can learn item-specific information (repeated triads) at a normal rate, even though their explicit memory is severely impaired. It is hypothesized that learning of item-specific information relies on repetition priming effects rather than on explicit memory processes.

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