Search PubMed⌕ Search

Biomedical subjects

M Vidailhet

Publications and source records attributed to M Vidailhet.

At least 109 records · Page 6Linked to original sources
PubMed1998

Cerebral Erdheim-Chester disease: report of two cases with progressive cerebellar syndrome with dentate abnormalities on magnetic resonance imaging.

Two patients with Erdheim-Chester disease with progressive cerebellar dysfunction and pyramidal signs are reported on. Cerebral MRI showed bilateral increased signal intensity in peridentatal regions on T2 weighted sequences. Both patients had kidney and bone involvement, established on bone biopsy for one. One patient improved with steroid therapy. This contrasts with previous reports, which describe rare neurological manifestations and the failure of different therapeutic approaches.

Adult↗
PubMed1998

Maturation of B cells in the lamina propria of human gut and bronchi in the first months of human life.

Little is known of the maturation of the mucosae-associated lymphoid tissue (MALT) in man, because, for ethical reasons, tissues from newborns are not easy to obtain. We used the opportunity provided by autopsies systematically performed in infants who died of Sudden Infant Death Syndrome (SIDS) to study the maturation of the MALT after birth. Gut and bronchus samples of 90 infants from postpartum to 90 months and who died from SIDS were collected and studied by histological and immunofluorescence examination. Plasma cells, absent at birth, appeared within a few hours after birth and initially were of the IgM isotype. IgA plasma cells appeared at 12 days. These cells were first observed in gut and later in bronchi, indicating that maturation of the gut precedes that of bronchi. The number of plasma cells increased rapidly over time and IgA plasma cells became predominant after 3 weeks in the gut and 6 weeks in bronchi. At birth, only small IgM bearing B-cell foci were seen and organized germinal centers appeared to develop over a few days, first in the gut and only later in bronchi. These results confirm that, in man, the MALT organization at birth is still in its fetal form and that maturation depends on intestinal challenges and evolves over several weeks before IgA becomes the predominant isotype secreted.

B-Lymphocytes↗
PubMed1998

Abnormal substrate levels that depend upon mitochondrial function in cerebrospinal fluid from Alzheimer patients.

BACKGROUND: Impaired oxidative and energy metabolism are important features in Alzheimer's disease. These metabolic abnormalities may induce functional disturbances and are associated with significant cognitive impairment. OBJECTIVE: To determine whether mitochondrial function is altered by Alzheimer's disease, a quantitative analysis of substrates that enter the tricarboxylic acid cycle was carried out in cerebrospinal fluid (CSF) from Alzheimer patients. METHODS: Organic acid levels related to carbohydrate oxidation were measured in CSF from patients affected by dementia of Alzheimer type (n = 17) and from nondemented elderly controls (n = 17) using a gas chromatography/mass spectrometry system. CSF glucose and glutamine concentrations were determined by a quantitative enzymatic method and by ion exchange chromatography, respectively. RESULTS: Compared to age-matched controls, patients had a higher CSF level of lactate (p = 0.002) and a lower mean level of succinate (p = 0.002), fumarate (p = 0.003) and glutamine (p = 0.0005). The CSF glucose level was not modified. CONCLUSION: Our results suggest an impairment of mitochondrial oxidative metabolism in brain cells of patients with Alzheimer's disease.

Aged↗
PubMed1998

[Clinical diagnostic criteria for multiple system atrophy].

What are the distinctive criteria for the diagnosis of multiple system atrophy? The combination of motor, dysautonomic, neuropsychological and eyes movements may help to distinguish, at a early stage, multiple system atrophy from other neurodegenerative diseases such as Parkinson's disease, progressive supranuclear palsy or corticobasal degeneration. Thus, these criteria are suitable both for clinical care and drug trials.

Cognition Disorders↗
PubMed1998

[Study of cortical atrophy with magnetic resonance imaging in corticobasal degeneration].

Corticobasal degeneration (C.B.D.) is a neurodegenerative disorder characterized mainly by an asymmetrical a kineto-rigid syndrome associated with fronto-parietal cortical signs, particularly apraxia. Conventional imaging even magnetic resonance imaging (M.R.I.) has often been considered as poorly contributive for the diagnosis of C.B.D. We retrospectively studied routinely performed M.R.I. scans of 15 patients presenting a clinical and metabolic (P.E.T/S.P.E.C.T.) syndrome characteristic of probable C.B.D. M.R.I. scans were assessed by 3 investigators, not aware of the clinically most affected side, taking into account M.R.I. technical parameters. We quantified, on each side, the cortical atrophy (frontal, parietal and temporal) and the white matter changes, by using the semi-quantified method of Victoroff et al. (1994). Abnormalities were considered if observed by at least 2 of the 3 investigators. Abnormalities were then correlated with the side initially and most severely affected. The most contributive findings were the asymmetric parietal atrophy (clinically correlated in 93 p. 100 of cases), asymmetric frontal atrophy (clinically correlated in 60 p. 100) and asymmetric dilatation of the lateral ventricles (clinically correlated in 60 p. 100). 80 p. 100 of affected subjects displayed at least 2 of these M.R.I. abnormalities. These results are in accordance with the metabolic and pathologic features of C.B.D. This study demonstrates that M.R.I. evaluation of the cortical atrophy asymmetry may contribute to the diagnosis of C.B.D.

Age of Onset↗
PubMed1997

[Dystonia].

Dystonia can be considered either as a symptom, or as a disease. An initial classification of dystonia can be made according to the localization and the severity of the spasms or the associated movement disorders such as myoclonus. A second classification differentiates idiopathic dystonia and secondary dystonia. Personnel medical history, familial cases, neurological symptoms such as pyramidal, cerebellar, oculomotor signs are helpful clues in the diagnosis strategy. Drugs, botulinum toxin, physiotherapy are often combined symptomatic treatment regardless of the cause of dystonia.

Adolescent↗
PubMed1997

[Tremors].

In this general review of tremors, one must distinguish the parkinsonian rest tremor, which concerns relaxed muscles, from other tremors that accompany muscle activities, such as maintaining a posture or executing a movement. Among various postural and action tremors, essential tremor occupies first place, in terms of its prevalence. The diagnosis of essential tremor is based on precise criteria. Often hereditarily transmitted, essential tremor can sometimes be quite disabling. Essential tremor and parkinsonian tremor are compared on an accompanying table. Other types of tremor are reviewed according to their possible prevalences. i.e. iatrogenic tremor and dystonic tremor. Particular attention is paid to orthostatic tremor, multiple sclerosis tremor and psychogenic tremor.

Humans↗
PubMed1997

Urinary disturbances in striatonigral degeneration and Parkinson's disease: clinical and urodynamic aspects.

Although urinary disturbances are more frequent in multiple system atrophy (MSA) than in Parkinson's disease (PD), the striatonigral degeneration (SND) type of MSA is difficult to distinguish from PD, especially when the latter is associated with orthostatic hypotension or urinary symptoms. The pattern of urinary symptoms and urodynamic dysfunction was analyzed in 15 SND and 35 PD patients with urinary complaints. In SND, dysuria with or without chronic retention, frequently associated with a hypoactive detrusor and low urethral pressure, permitted early and reliable diagnosis. In PD, urgency to void, with or without difficulty voiding, but without chronic retention, associated with detrusor hyperreflexia and normal urethral sphincter function, predominated. In clinical practice, the study of urinary symptoms and bladder function may help to distinguish SND from PD in patients with urinary disturbances.

Aged↗
PubMed1997

Memory for spatial location in 'de novo' parkinsonian patients.

A deficit in memory for spatial location was recently reported in typical non-demented parkinsonian patients ('standard'). Is this deficit related to dopamine depletion? Such an association would reinforce the suggestion that striato-frontal neuronal circuits are implicated in memory for item-specific spatial coordinates. To answer this question, we compared the performance of 10 recently diagnosed and not yet treated parkinsonian patients ('de novo'), in which the neurobiochemical deficit is considered to involve mainly the nigrostriatal dopaminergic system, to that of 14 controls matched for age, global cognitive efficiency and mood, on a visuospatial learning test. The task required little motor or constructive functions and was designed to allow control of encoding and comparison of free recall, cued recall and recognition. Compared to controls, 'de novo' patients displayed a lower performance in memory for visuospatial location of pictures, contrasting with relative preservation of verbal memory, perceptive visuospatial and executive functions. These results confirm the sensitivity of visuospatial memory even at an early stage of Parkinson's disease and suggest the implication of the nigrostriatal dopaminergic system, and associated striato-frontal neuronal circuits, in executive processes needed for spatial location learning.

Analysis of Variance↗
PubMed1997

Low-dose clozapine improves dyskinesias in Parkinson's disease.

The severity of parkinsonian motor disability and dyskinesias was evaluated in seven levodopa-responsive patients with Parkinson's disease after an acute challenge with the mixed dopamine agonist apomorphine, before and after low-dose clozapine (50 mg) for 18 +/- 2 days. There was a significant 59% improvement (p < 0.05) of apomorphine-induced dyskinesias without aggravation of parkinsonian motor disability following clozapine treatment. The results suggest that low-dose clozapine, already shown to improve psychotic symptoms, may help to reduce severe levodopa-induced dyskinesias in parkinsonian patients.

Aged↗
PubMed1997

Pallidal stimulation for Parkinson's disease. Two targets?

There has been renewed interest in functional surgery as treatment for Parkinson's disease (PD). Although pallidotomy and chronic pallidal stimulation are highly effective in suppressing levodopa-induced dyskinesia (LID), both methods also seem to be effective in reducing parkinsonian disability. However, the simultaneous improvement of LID and motor signs is hard to explain with the classic model of basal ganglia circuitry. Taking advantage of the fact that deep brain stimulation is reversible and that implanted electrodes contain four discrete stimulation sites, we investigated the effect of stimulation on different sites of the globus pallidus (GP) in five PD patients. Stimulation in the dorsal GP (upper contact) significantly improved gait, akinesia, and rigidity and could induce dyskinesia when patients were in the "off" state. In contrast, stimulation in the posteroventral GP (lower contact) significantly worsened gait and akinesia, although the reduction in rigidity remained. For patients in the "on" state, stimulation in the posteroventral GP dramatically reduced LID but, as in the "off" state, worsened gait and akinesia, thus canceling out the antiparkinsonian effect of levodopa. Our results indicate that stimulation had a striking different effect on parkinsonism and dyskinesia when applied at two different loci of the GP and that stimulation applied in the posteroventral GP produced opposite effects on rigidity and on akinesia. We conclude that parkinsonian signs and LID are a reflection of at least two different anatomofunctional systems within the GP and that this functional organization of the GP needs to be considered when determining the optimal target for surgical treatment of PD.

Adult↗
PubMed1996

Striatopallidal and thalamic dystonia. A magnetic resonance imaging anatomoclinical study.

OBJECTIVE: To determine which brain structures are involved in symptomatic unilateral dystonia caused by localized cerebral infarction. DESIGN: Three-dimensional T1-weighted magnetic resonance imaging sequence and stereotactic analysis were used to analyze the topography of the lesions. Stereotactic localization of thalamic lesions was conducted according to the atlas of Hassler with a Voxtool software (Advantage Windows Workstation, General Electric, Milwaukee, Wis) workstation system. PATIENTS: Eight patients with hemidystonia, segmental dystonia, or focal dystonia were selected from among 51 consecutive patients (between January 1988 and May 1993) with symptomatic unilateral dystonia. RESULTS: Patients had dystonic spasms (n=4) or myoclonic dystonia (n=4). Lesions associated with dystonic spasms were located in the striatopallidal complex, and those with myoclonic dystonia were in the thalamus contralateral to the dystonia. Lesions of the striatopallidal complex involved the putamen posterior to the anterior commissure in all patients and extended variably into the dorsolateral part of the caudate nucleus, the posterior limb of the internal capsule, or the lateral segment of the globus pallidus. These lesions were centered in the "sensorimotor" part of the striatopallidal complex, with a trend toward a somatotopical distribution. Lesions of the thalamus were located in the ventral intermediate and ventral caudal nuclei, while the ventral oral anterior and posterior nuclei (which receive pallidal efferents) were largely spared. CONCLUSIONS: These results suggest that striatopallidal and thalamic dystonia may have different pathophysiologic bases.

Adolescent↗
PubMed1996

[Sleeping position, prevention of sudden death syndrome and gastroesophageal reflux].

Based on results of epidemiological studies, dorsal or lateral sleeping positions are now recommanded in the prevention of sudden infant death syndrome (SIDS). This raises an ethical question about the attitude towards the ventral positioning therapy for gastroesophageal reflux (GOR). The consensus conference considers that the ventral position should only be recommanded in GOR when the benefit appears to outweigh the risk of SIDS that it induces. The conference proposes that for infants with simple uncomplicated reflux, sleeping in the prone position should not be introduced in the first line treatment. Prone positioning should be restricted to complicated cases resistant to dietary and medical measures.

Gastroesophageal Reflux↗
PubMed1996

[Pregnancy and the child of a mother with phenylketonuria].

Pregnant women with hyperphenylalaninemia are at high risk of spontaneous abortion and of giving birth to infants with congenital malformations, microcephaly and mental defect. Among mothers whose phenylalaninemia is greater than 1200 mumol/L (20 mg/100 mL), 95% have at least one child with mental retardation. A low phenylalanine diet with a good control of phenylalaninemia, started before conception, reduces this risk, better results being obtained when plasma phenylalanine levels are maintained below 360 mumol/L (6 mg/100 mL) as compared with levels maintained between 360 to 600 mumol/L (6-10 mg/100 mL). Thus, systematic contraception and planned pregnancies must be recommended in all hyperphenylalanemic young women. This implies early information of phenylketonuric teenage girls and their parents. In addition, efforts must be made to join and inform all women having had hyperphenylalaninemia at birth, whether they received a dietary treatment or not. It is also important that general practitioners, pediatricians and obstetricians be aware of the high recurrence risk in hyperphenylalanemic women who gave birth to a microcephalic or malformed infant.

Female↗
PubMed1996

Saccade disturbances after bilateral lentiform nucleus lesions in humans.

OBJECTIVE: To determine the roles of the putamen and pallidum in ocular motor control. METHODS: Eye movements were recorded electro-oculographically in nine patients with bilateral focal lesions affecting the lentiform nucleus, and in 12 age matched control subjects. Reflexive visually guided saccades (gap task), antisaccades, memorised sequences of saccades, memory guided saccades (with visual input only, and with both visual and vestibular inputs), and predictive saccades (with and without gap) were studied. RESULTS: Latency and accuracy of visually guided saccades were normal. The percentage of errors in the antisaccade task and latency of correct antisaccades did not differ significantly from the results of controls. The percentage of errors in saccade sequences was significantly increased. Accuracy of the two types of memory guided saccades was impaired bilaterally. The percentage of predictive saccades was significantly decreased when a gap existed, but unchanged without a gap, compared with controls. Therefore, saccades made immediately in response to an external target (reflexive visually guided saccades and antisaccades) were performed without difficulty, whereas those requiring an internal representation of such a target (such as memory guided saccades, predictive saccades, and saccade sequences) were performed with significant disturbances. CONCLUSIONS: The lentiform nucleus influences the cortical areas involved in the control of saccades when the experimental paradigm requires the use of an internal representation of the target for correct planning and execution of the ensuing saccade.

Adult↗
PubMed1996

Improvement of levodopa-induced dyskinesia by propranolol in Parkinson's disease.

Seven patients suffering from Parkinson's disease (PD) with severely disabling dyskinesia received low-dose propranolol as an adjunct to the currently used medical treatment. There was a significant 40% improvement in the dyskinesia score without increase of parkinsonian motor disability. Ballistic and choreic dyskinesia were markedly ameliorated, whereas dystonia was not. This study suggests that administration of low doses of beta-blockers may improve levodopa-induced ballistic and choreic dyskinesia in PD.

Adrenergic beta-Antagonists↗