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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
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↗
PubMed1987

Acetylcholinesterase and butyrylcholinesterase activity in the cerebrospinal fluid of patients with neurodegenerative diseases involving cholinergic systems.

Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were assayed in the cerebrospinal fluid (CSF) of subjects with neurodegenerative diseases (dementing and non-dementing, with and without known cholinergic lesions), to determine whether CSF AChE is a valid marker of central cholinergic activity. The relative proportions of the different forms of each enzyme and of AChE to BChE were similar in CSF and brain. AChE decreased in Huntington's chorea (degeneration of striatal cholinergic interneurons) but also in multiple sclerosis (not known to affect cholinergic systems). BChE paralleled AChE, although the enzymes were dissociated in some patients. It is concluded that CSF AChE activity may globally reflect brain AChE, but pathology-induced changes may not be directly reflected.

Acetylcholinesterase↗
PubMed1986

Disappearance of parkinsonian signs after spontaneous vascular 'thalamotomy'.

Disappearance of parkinsonian symptoms was observed in a 57-year-old patient with Parkinson's disease after a contralateral thalamopeduncular infarct. From analysis of stereotaxic data in parkinsonian patients, this may be explained by lesion of the ventro-oral internal nucleus or of Forel's field, both of which are involved in thalamopeduncular infarcts.

Female↗
PubMed1986

Human autonomy and the frontal lobes. Part I: Imitation and utilization behavior: a neuropsychological study of 75 patients.

A type of pathological behavior, imitation behavior (IB), is newly described. In this behavior patients imitate the examiner's gestures, although not instructed to do so. Patients explain that they thought they had to imitate the examiner. IB is the first stage of utilization behavior (UB). Neuropsychological examination of 40 patients with IB, of 35 with UB, and of 50 disease controls demonstrates the existence of a frontal syndrome and two determining features of such behavior: dependence on (1) the social and (2) the physical environments. Loss of intellectual control was also required for the occurrence of such behavior. UB and/or IB were present in 96% of the 29 patients with focal lesions of the frontal lobes. Computed tomographic scans in 26 of these patients showed involvement of the inferior half of the anterior part of one or both frontal lobes. IB and UB are interpreted as release of parietal lobe activities, resulting from impairment of frontal lobe inhibition.

Behavior↗
PubMed1986

Heterogeneity of cognitive impairment in progressive supranuclear palsy, Parkinson's disease, and Alzheimer's disease.

Patterns of cognitive and behavioral impairment were analyzed in patients with progressive supranuclear palsy (PSP), Parkinson's disease (PD), and senile dementia of Alzheimer's type (SDAT), matched for age, sex, manual laterality, educational level, and degree of intellectual deterioration. The scores of the three groups of patients were significantly lower than those of controls and were comparable on tests of verbal and visuospatial functions as well as global memory. Patients with SDAT could be distinguished by the severity of verbal memory disorders; patients with PSP, and to a lesser degree those with PD, by impaired performances on tests sensitive to frontal lobe dysfunction.

Aged↗
PubMed1982

[Loss of psychic self-activation. Compulsive activity of obsessional type. Bilateral lenticular lesion (author's transl)].

After a carbon monoxide intoxication with coma of short duration, a 25 years-old man sustained a demential state and during the first weeks, a mild extrapyramidal syndrome. One year later, the mental state had progressively improved, although with a severe anterograde amnesia but the clinical picture had become unique. Let without external stimulation, the patient remained inert without any activity, often lying on his bed but not sleeping. He had lost any initiative. At the opposite, if he was stimulated, his physical, intellectual and affective performances were nearly normal, verbal fluency remaining however poor. Psychic self-activation appeared to be lost but psychic possibilities after external stimulation were nearly normal. When inactive, the patient was occupied with a mental compulsive activity. C.A.T. showed bilateral necrotizing lesions in the globus pallidus. The present case is very similar to a previously reported one. (D. Laplane et al., Rev. Neurol., 1981, 137 : 269-276) in which bilateral lenticular lesions produced the same syndrome. The pallidal area seems to play a determinant role in the processes of self-activation of psychic life.

Adult↗