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Biomedical subjects

B Pillon

Publications and source records attributed to B Pillon.

At least 91 records · Page 5Linked to original sources
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.

Aged↗
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.

Aged↗
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.

Aged↗
PubMed1990

Age-induced cognitive disturbances in Parkinson's disease.

We investigated the influence of age on the occurrence of cognitive disturbances in Parkinson's disease (PD), by evaluating neuropsychological performances in early- and late-onset groups of patients (less than 45 and greater than 65 years, respectively), individually paired for all the variables of parkinsonism and compared with age-matched controls. Cognitive disorders were limited in the early-onset PD group compared with their age-matched controls. Conversely, we found global cognitive changes, including marked frontal lobe dysfunction, in the late-onset group. This specific cognitive impairment in older patients related to a significant interaction between the aging and disease processes. Late onset seemed to compound the subtle cognitive changes associated with the disease for which the early-onset group compensated. This compounding effect of aging may explain, at least partially, the high frequency of dementia in older PD patients.

Adult↗
PubMed1989

Lateral visually-guided saccades in progressive supranuclear palsy.

Lateral visually-guided saccades were studied electro-oculographically in 40 patients with progressive supranuclear palsy (PSP) in order to increase understanding of the pathophysiology of the oculomotor syndrome and the suprareticular control of saccades. In the two main paradigms used, the central fixation point was removed just before the appearance of a lateral target, the subject being told either to look at the target (gap task) or, particularly to test frontal lobe influence, in the direction opposite to the target (antisaccade task). Saccade latency distribution in the gap task was significantly more scattered in patients as compared with 40 normal control subjects, although mean latencies did not differ greatly. In particular, many patients had latencies shorter or longer than those of control subjects. In the PSP group, the percentage of errors in the antisaccade task (misdirected saccades made towards the target) was strongly correlated with latency in the gap task, high percentages of errors corresponding to short latencies. There was also a correlation between latency and the frontal dysfunction evaluated by neuropsychological tests. These correlations suggest that short latencies could result from a severe impairment of the frontal inhibitory system involved in saccade initiation. Long latencies would result from damage to diverse excitatory suprareticular pathways (such as the superior colliculus) or to circuits responsible for shifts in visual attention. Lastly, 20 patients were followed longitudinally (for 3-12 months). The initially great intersubject variability of saccade latency in the gap task significantly decreased over a period of several months. This finding could result from a secondary balance between the impairment of the frontal inhibitory system and that of the diverse excitatory pathways.

Aged↗
PubMed1989

Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study.

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.

Adult↗
PubMed1989

Does cognitive impairment in Parkinson's disease result from non-dopaminergic lesions?

In order to investigate the neuronal basis of cognitive disorders in Parkinson's disease, the neuropsychological performance of 120 patients with idiopathic Parkinson's disease was analysed in relation to motor symptoms as a function of their response to levodopa. Cognitive impairment was poorly correlated with akinesia and rigidity, symptoms which respond well to levodopa treatment, and was not correlated at all with that part of the patients' motor score that could be improved by the drug. In contrast, strong correlations were found between all neuropsychological test scores and axial symptoms such as gait disorder and dysarthria, which respond little if at all to levodopa treatment. The neuropsychological test scores were also strongly correlated with the motor score of patients estimated when clinical improvement was maximal under levodopa treatment. This score is assumed to represent residual non-dopaminergic motor dysfunctions. The correlations suggest that much of the cognitive impairment in Parkinson's disease results from the dysfunction of non-dopaminergic neuronal systems.

Adult↗
PubMed1989

Increased wave P 300 latency in progressive supranuclear palsy.

The visually evoked P 300 wave and related reaction times (RTs) were studied in 25 patients with progressive supranuclear palsy (PSP). Both the P 300 wave latency and the RTs were significantly increased compared with 14 control subjects, and were correlated with an intellectual deterioration index calculated from neuropsychological scores. It is suggested that the study of wave P 300 may contribute to the diagnosis of cognitive disorders in PSP.

Aged↗
PubMed1989

Cognitive slowing in Parkinson's disease fails to respond to levodopa treatment: the 15-objects test.

To evaluate clinically the slowing of cognitive processing in Parkinson's disease, we used a visual discrimination task consisting of 15 superimposed images of objects. The time needed to identify 12 objects increased by 58% in 70 patients withdrawn from levodopa treatment compared with 20 controls matched for age and education. Perceptual, motor, and psycholinguistic factors, as well as mood, only partially accounted for the slowness of performance. The 15-objects test scores of the parkinsonian patients correlated significantly with both their intellectual impairment and the severity of their parkinsonian disability, but not with the duration of the disease. The scores did not correlate with depression. Levodopa had no effect on the score, although the parkinsonian motor disability score was improved by 54%. The results indicate a cognitive slowing in Parkinson's disease which is probably related to abnormalities of nondopaminergic neuronal systems in the brain.

Adolescent↗
PubMed1988

Slowing of cognitive processing in progressive supranuclear palsy. A comparison with Parkinson's disease.

To investigate central processing time in patients with progressive supranuclear palsy and Parkinson's disease, reaction times were measured using tasks with different levels of cognitive complexity but with the same motor response. In patients with Parkinson's disease, the additional central processing time required for more complex situations was no different from that in control subjects, suggesting that cognitive aspects of the reaction time procedures tested were possibly too simple to reveal a slowing of thought processes in these patients. Conversely, the central processing time was increased in patients with progressive supranuclear palsy compared with both Parkinson's disease and control subjects. The increase was associated with impairment in frontal lobe test performance. These results confirm that a slowing of central processing is a prominent feature of the cognitive disturbances of progressive supranuclear palsy and, furthermore, suggest that this slowing may be related to striatofrontal dysfunction.

Aged↗
PubMed1988

[Loss of psychic self-activation and stereotyped mental activity caused by a frontal lesion. Relation of the obsessive-compulsive disorder].

A case of frontal lobe lesions is reported, its interest being that it is similar to a syndrome that we have previously described as the consequence of lenticular nucleus lesions. This syndrome includes primarily a loss of psychic self-activation (psychic akinesia) and compulsive or pseudo-compulsive activities. In the present case the lesions involved the deep white matter of the prefrontal cortex on both sides, and were most extensive in the depth of the middle frontal gyrus. This similitude brings further support to the notion that subcortical damage of the lenticular nuclei can induce a frontal-like syndrome. The similitude with some of the behavioural aspects or depressive of hebephrenic states is emphasized. The occurrence of stereotyped mental activities is the basis for a discussion of the relationships with some features of obsessive-compulsive neurosis.

Activities of Daily Living↗
PubMed1987

Alexia without agraphia in a left-handed patient with a right occipital lesion.

A left-handed patient who had suffered an ischemic vascular accident in the territory of the right posterior cerebral artery displayed alexia without agraphia. Clinical examination of this alexia revealed semiological characteristics comparable with those observed in cases of left temporo-occipital lesions in right-handed patients. Analysis of these disturbances indicated that they were agnosic in nature. The associated disturbances included problems of visual representation and topographic memory together with an amnesic syndrome.

Aged↗
PubMed1987

Cholinergic-dependent cognitive deficits in Parkinson's disease.

In a double-blind cross-over study, the effects of a subthreshold dose of scopolamine (0.25 mg) on memory were compared in 32 control subjects and 32 parkinsonian patients who were without any sign of intellectual and mnemic impairment. Although the scores of the controls in the memory test battery showed no deterioration after the administration of scopolamine, the same dose resulted in significantly reduced memory performance in parkinsonian patients in two tests which involved the recognition of meaningless drawings. The selective vulnerability of parkinsonian subjects without cognitive impairment to a subthreshold dose of scopolamine suggests the existence of an underlying alteration of central cholinergic transmission. The neuropsychological findings in our study agree with postmortem biochemical data, which showed decreased cortical choline acetyltransferase activity in all parkinsonian patients, suggesting the existence of neuronal compensation in parkinsonian patients who are without cognitive impairment.

Acetylcholine↗