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B Pillon

Publications and source records attributed to B Pillon.

At least 73 records · Page 4Linked to original sources
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

Delusional misidentification: a clinical, neuropsychological and brain imaging case study.

The case of a young woman with a disorder involving Capgras syndrome, Frégoli syndrome, intermetamorphosis, and the subjective-doubles syndrome is reported. Neuropsychological assessment showed a low efficiency in the complex visuospatial organization tasks and in non-verbal memory. MRI found a left lenticular hypodensity, and two PET scans performed in the symptomatic and recovered states showed significant changes and asymmetries in cerebral glucose metabolism in the frontal, parietal, and subcortical regions. These findings are discussed with respect to recent models of delusional misidentification syndromes.

Adult↗
PubMed1994

Impaired simultaneous cognitive task performance in Parkinson's disease: a dopamine-related dysfunction.

Patients with Parkinson's disease (PD) have trouble programming two separate motor acts concurrently. We tested the hypotheses that (1) PD patients may also have difficulty processing two cognitive tasks simultaneously, and (2) the expected deficit may be related to the striatal dopaminergic depletion. We used auditory and visual choice reaction time (CRT) tasks, presented either separately or concurrently, and compared the performance of three groups of PD patients: a group of patients under their usual dose of levodopa ("standard"); a group assessed both at the time of maximal clinical benefit ("on" state) and at the time of minimal clinical benefit (treatment withdrawn for about 18 hours; "off" state); and a group of recently diagnosed untreated patients ("de novo"). Compared with controls, standard and "on" state patients had a normal performance for both separate and concurrent CRT tasks. In contrast, "off" state and de novo patients had a normal performance in the separate CRT tasks but significant deficits in the concurrent CRT tasks. These results suggest that adequate dopaminergic transmission is necessary for concurrent processing of cognitive information and that the striatum integrates the sensorimotor information required to program cognitive acts.

Acoustic Stimulation↗
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.

Animals↗
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

Time for reorienting of attention: a premotor hypothesis of the underlying mechanism.

The paradigm of the covert orienting of attention (COA) has shown that the displacement of visual attention may be assessed even in the absence of eye movement. Stimuli correctly cued before their presentation are usually detected faster than uncued stimuli. However, miscued stimuli induce an increased detection time, which has been attributed to the time required for the reorientation of attention from the incorrect to the correct spatial location. Currently, the mechanism of such a displacement of visual attention remains unknown. Rizzolatti et al. Neuropsychologia 25, 31-40 (1987) have suggested a premotor hypothesis which suggests that an oculomotor disprogramming and reprogramming is necessary to reorient visual attention, even if the eye movement is inhibited. Since shifting of auditory attention from one ear to the other does not require any motor control, we further investigated the model of COA in 20 normal subjects who performed two tasks requiring a reorienting of auditory attention: (1) a choice RT task that requires a response readjustment during the auditory reorienting; (2) a simple RT task that does not require a response readjustment during the auditory reorienting; (2) a simple RT task that does not require a response readjustment during the auditory reorienting. Results indicate that correctly cued stimuli significantly reduce the RT in both tasks and that this reduction is greater in the choice than in the simple RT task. This suggests that a correct cue may produce a pre-programming of the response, in addition to the pre-engagement of the perceptual attention.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1993

Delayed response tasks and prefrontal lesions in man--evidence for self generated patterns of behaviour with poor environmental modulation.

The functions of the frontal lobes in humans are still under debate, mainly because none of the neuropsychological tests used for their assessment is sufficiently specific for frontal dysfunction. In animals, the delayed reaction paradigm is considered to be a specific marker of the function of dorsolateral region of the prefrontal cortex. It seemed of interest, therefore, to attempt to apply this paradigm to patients with recent and limited cortical lesion of vascular origin. The performance of patients with dorsolateral prefrontal lesion (n = 10) was compared to that of patients with post-central lesion (n = 10) and control subjects (n = 24), in four experiments: a Delayed Response task in which the correct answer was previously indicated by an explicit cue (externally guided task); Delayed Alternation and Non-Alternation tasks coupled with a Delayed Reversal task in which the patient had to discover the rule by himself in the absence of explicit cues (internally driven tasks). Patients with prefrontal lesion showed a specific deficit in the Delayed Response task, the emergence of a stereotyped behaviour in the Delayed Alternation task and an inability to deduce and to transfer rules (non-alternation and reversal), mainly because of difficulty in abandoning previous behaviours. Our study demonstrates that the prefrontal cortex plays a role in behavioural adaptation to challenging new situations by inhibiting not only ongoing elaborated programmes but also the emergence of previously established automatic programmes. The respective role of the prefrontal cortex and the basal ganglia in these two levels of behavioural organization is discussed.

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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.

Affect↗
PubMed1993

Loss of brain 5-HT2 receptors in Alzheimer's disease. In vivo assessment with positron emission tomography and [18F]setoperone.

Using [18F]setoperone and positron emission tomography (PET), alterations in serotonergic 5-HT2 receptor binding were studied in cerebral cortex of nine unmedicated patients with probable Alzheimer's disease and 37 healthy controls. The kinetics of unchanged radioligand in plasma and 18F-radioactivity in blood and brain were obtained for 90 min following tracer injection. The specific binding of [18F]setoperone to 5-HT2 receptors in the cerebral cortex was quantitated by subtraction using cerebellum as reference. In controls, a significant reduction in specific binding was associated with age and similar linear regression slopes were obtained in all the cortical regions studied. No significant difference was observed between patients with Alzheimer's disease and age-matched controls in the injected mass of setoperone, percentage of unmetabolized [18F]setoperone in plasma, 18F-radioactivity in blood fractions and cerebellar 18F-radioactivity concentration, indicating similar non-specific brain kinetics and metabolism of the radioligand. In contrast, there was a significant reduction in specific [18F]setoperone binding in the cerebral cortex in patients with Alzheimer's disease relative to control values (temporal, 69%; frontal, 69%; parietal, 55%; temporo-parietal, 54%; occipital cortex, 35%). The results demonstrate that the loss in 5-HT2 receptor binding in the cerebral cortex of patients with Alzheimer's disease, long documented by post-mortem studies, can now be assessed in vivo using PET.

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PubMed1992

Corticobasal degeneration: decreased and asymmetrical glucose consumption as studied with PET.

Cerebral energy metabolism was studied by positron emission tomography and [18F]fluorodeoxyglucose in five patients with clinical diagnoses of probable corticobasal degeneration. A reduction in glucose consumption was observed in most cortical and subcortical structures compared to age-matched controls. The reduction was greatest on the side of the brain contralateral to the most affected limbs, as shown by the significantly lower ratios of contralateral to homolateral metabolic rates, in the temporal and sensorimotor cortex of patients compared to controls. A distinct asymmetry between the two hemispheres could be observed in a patient who was examined twice in the course of his illness. Detection of this asymmetrical decrease in brain cortical and subcortical glucose metabolism may prove useful as additional evidence supporting clinical diagnoses of the disease.

Aged↗
PubMed1992

Cognitive function, insulin-dependent diabetes and hypoglycaemia.

A series of seven psychometric tests, to evaluate mental concentration and the ability to retain selective attention, lexical fluency, wordlist memorizing and psychomotor speed, was performed on 25 non-diabetic control subjects and 55 insulin-dependent diabetes (IDD) patients of similar social background and professional status. When tested, none of the diabetics was hypoglycaemic and these patients were divided into two groups: Group I: 30 IDD patients unaware of hypoglycaemia, and experiencing frequent and severe episodes of hypoglycaemia. Group II: 25 IDD patients aware of hypoglycaemia. Groups I and II had experienced the disease for the same period of time (17 +/- 13 vs. 14 +/- 11 years, respectively) and they had similar HbA1c levels (7.14 +/- 1.25% vs. 8.6 +/- 1.88%, respectively) and degenerative complications. Compared with the scores of the controls, the Group I scores were lower in four tests: trail-making part A (psychomotor speed; P less than 0.001) and part B (retaining selective attention; P less than 0.01), lexical fluency (P less than 0.01) and Rey auditory-verbal learning test (wordlist learning; P less than 0.05). Group II scores were lower in two tests: trail-making part A (P less than 0.01) and part B (P less than 0.05). In word memorizing, the performance of Group I was inferior to that of Group II (P less than 0.05). In general, these psychometric tests showed that IDD scores were lower than those of the controls, with an average of 67% for Group II and 80% for Group I. Chronic hyperglycaemia and severe hypoglycaemia may have a deleterious effect on cognitive performance. In particular, several severe episodes of hypoglycaemia could be responsible for permanent memory impairment.

Adolescent↗
PubMed1991

Severity and specificity of cognitive impairment in Alzheimer's, Huntington's, and Parkinson's diseases and progressive supranuclear palsy.

To investigate differences in severity and specificity of cognitive impairment among various neurodegenerative diseases, we tested groups of patients presenting with senile dementia of the Alzheimer's type (SDAT) (n = 44), progressive supranuclear palsy (PSP) (n = 45), Huntington's disease (HD) (n = 35), and Parkinson's disease (PD) (n = 164), with an extensive neuropsychologic battery. We found dementia, as defined by a global intellectual performance 2 SD lower than mean control values, in 93% of patients with SDAT, 66% of patients with HD, 58% of patients with PSP, and 18% of patients with PD. Specific features of cognitive impairment distinguished the four groups of patients once they were matched for level of intellectual deterioration. This study shows the frequency of dementia in predominantly subcortical degenerative diseases and indicates that "subcortical dementia," rather than being a homogeneous entity, should be divided into specific subtypes of cognitive impairment related to different underlying pathology.

Alzheimer Disease↗
PubMed1991

Severity and specificity of cognitive impairment in Alzheimer's, Huntington's, and Parkinson's diseases and progressive supranuclear palsy.

To investigate differences in severity and specificity of cognitive impairment among various neurodegenerative diseases, we tested groups of patients presenting with senile dementia of the Alzheimer type (SDAT; 44), progressive supranuclear palsy (PSP; 45), Huntington's disease (HD; 35) and Parkinson's disease (PD; 164), with an extensive neuropsychological battery. We found dementia, as defined by a global intellectual performance 2 standard deviations lower than mean control values, in 93% of SDAT, 66% of HD, 58% of PSP, and 18% of PD patients. Specific features of cognitive impairment distinguished the four groups of patients once they were matched for level of intellectual deterioration: remote memory and linguistic disorders in SDAT, frontal lobe-like abnormalities in PSP, concentration and acquisition disorders in HD. There was no specific alteration in demented PD patients. This study demonstrates the frequency of dementia in predominantly subcortical degenerative diseases and indicates that "subcortical dementia," rather than being a homogeneous entity, should be divided into specific subtypes of cognitive impairment related to different underlying specific lesions of each disease.

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PubMed1990

Positron emission tomography study in progressive supranuclear palsy. Brain hypometabolic pattern and clinicometabolic correlations.

In 41 patients with progressive supranuclear palsy (PSP) that was diagnosed on the basis of eight clinical criteria (25 patients with all eight criteria [probable PSP] and 16 with six or seven criteria [possible PSP]), we studied cerebral energy metabolism by using positron emission tomography and the fludeoxyglucose F 18 or the oxygen 15 method. Compared with age-matched controls, each of the cortical and subcortical metabolic values was significantly reduced, with a predominance in the frontal cortex, in both groups of patients with probable and possible PSP, without a difference between these two groups, suggesting similar underlying disease. The frontal metabolic value decreased with disease duration, but the relative frontal hypometabolism (expressed as the fronto-occipital metabolic ratio) was apparently already present in the early stages of the disease. The parkinsonian motor score was correlated with the caudate and thalamic metabolic values. The intellectual deterioration index was significantly correlated with both the frontal and the nonfrontal metabolic values. Finally, the frontal neuropsychological score was significantly correlated with only the fronto-occipital metabolic ratio. Hence, in PSP, a degenerative brain disease with subcortical lesions, the prominent frontal lobe-like syndrome essentially depends on the relative hypometabolism of the frontal cortex.

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