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L Defebvre

Publications and source records attributed to L Defebvre.

At least 19 recordsLinked to original sources

Changes in oscillatory cortical activity related to a visuomotor task in young and elderly healthy subjects.

OBJECTIVE: In order to better understand the spatio-temporal interaction of the activated cortical areas when the movement is visuo-guided and to assess the age effect on the spatio-temporal pattern of cortical activity, we have compared a proximo-distal movement with visual-motor control and hand-eye coordination (targeting movement) with a distal and a proximal movement. METHODS: Brain's electrical activity was studied using the analysis of event-related (de)synchronizations (ERD/S) of cortical mu and beta rhythms in 17 subjects, 8 young and 9 elderly subjects. RESULTS: In both populations, we found an earlier and broader mu and beta ERD during the preparation of the targeting movement compared to distal and proximal movements, principally involving the contralateral parietal region. During the execution, a spreading over the parietocentral region during proximal movement and over the parietal region during targeting movement was observed. After the execution of proximal and targeting movements, a wider and higher beta ERS was observed only in the young subjects. In the elderly subjects, our results showed a significant decrease of beta ERS during the targeting task. CONCLUSIONS: These results suggest there was a larger recruitment of cortical areas, involving notably the parietal cortex when the movement is visuo-guided. Moreover, cerebral aging-related changes in the spatio-temporal beta ERS pattern suggests an impaired sensory integration.

Adult↗

[Neurophysiology of parkinsonian syndromes].

Neurophysiological investigations may contribute to establish the diagnosis of different parkinsonian syndromes such as multiple system atrophy, progressive supranuclear palsy and corticobasal degeneration, which are often suspected in case of atypical parkinsonian syndrome. They provide a means of objective analysis of certain symptoms (myoclonus for example) and identify the pathophysiological processes underlying these parkinsonian syndromes. This article reviews especially the following electrophysiological tests: autonomic nervous system analysis (sympathetic sudomotor skin response, R-R interval variation, electromyography of the external anal sphincter), surface electromyography and movement recording to investigate myoclonus, somatosensory and motor evoked potentials, brainstem reflexes (mainly the blink reflex), startle reaction, monosynaptic and long latency reflexes and finally the premotor potentials (contingent negative variation, Bereitschaftspotential) and movement-related desynchronization).

Anal Canal↗

[Clinical and electrophysiological features of "cortical tremor"].

The purpose of this paper is to draw attention to one particular variant of tremor named "cortical tremor," which corresponds to rhythmic cortical myoclonus whose principal differential diagnosis is essential tremor. Diagnosis may be established with electrophysiological explorations (electromyography, accelerometry, electroencelography with back averaging, long latency reflexes, giant somesthesic evoked potentials). Clinical and electrophysiological features of 15 patients are reported and compared to cases previously published. Association with generalized or partial seizures is possible. Other cases in the family are often mentioned with a dominant autosomal transmission. The therapeutic approach is based on the use of antiepileptic drugs.

Adolescent↗

[Postural strategies and falls in elderly and in parkinsonism].

OBJECTIVE: To use a posture analysis to show the evolution of postural pattern connected with falls. MATERIAL AND METHOD: It is a prospective study on two groups of 16 persons of more than 60 years. A group concerns 16 small disability off drug parkinsonian patients, a group concerns 16 healthy witnesses. All the persons benefited from a posture recording by means of a force platform and were followed during 1 year. RESULTS: Data analysis underlines three groups of persons corresponding to three postural patterns, independently of the presence of Parkinson disease. A group (n = 18) did not contain fallers, the second (n = 10 ) contained 20% of fallers, the third (n = 4) contained 100% of fallers. Differences between the groups were identified on 16 posturographic parameters. DISCUSSION: A group has a good functional value and one does not record any fall. Its characteristics, which correspond to a category of persons who compensate well for the phenomena of ageing, are found in the literature. A group has an intermediate functional value and regrets 20% of fallers. Kinetic profile reveals a tendency to the stiffness of the posture. This group is going to operate rather ankle strategies. A group has an inferior functional value and regrets 100% of fallers. Kinetic profile seems disrupted and not to be able to adapt itself in a satisfactory way to the situation otherwise than by stereotypical reactions. This group is going to operate systematically much less stabilizing hip strategies. CONCLUSION: A close determinism between physiological neuromotor ageing and Parkinson disease does exist. We showed with a prospective follow-up, the arisen of fall and showed the evolution of postural patterns related to fall. It appears as well that evolution mainly follows three stages leading from a small risk of fall gait pattern to a major risk of fall gait pattern.

Accidental Falls↗

Influence of internal globus pallidus stimulation on motor cortex activation pattern in Parkinson's disease.

OBJECTIVES: Indications of the functional neurosurgical treatments become more and more numerous, however, few methods were used to study the mechanism of action and some discrepancies came to light. We assessed the influence of internal globus pallidus (GPI) stimulation and L-Dopa on cortical activation during the preparation and execution phases of the movement compared to clinical improvement of Parkinson's disease. METHODS: We recorded the movement-related cortical potential and movement-related desynchronization. RESULTS: The Unified Parkinson's Disease Rating Scale was improved by 46% under stimulation and 64% under stimulation with L-Dopa. Premovement desynchronization was significantly increased on central contralateral derivation under stimulation with L-Dopa and decreased on frontocentral ipsilateral derivation under stimulation with and without L-Dopa. Movement desynchronization was improved on the contralateral motor cortex under stimulation with and without L-Dopa (benefit correlated with bradykinesia improvement). The movement-related postmotor potential was significantly increased under stimulation with L-Dopa. CONCLUSIONS: GPI stimulation alone influenced the premotor cortex activation during the planning and induced a selective and focal effect on the organisation of motor cortical activity during the movement execution which may explain bradykinesia improvement. The motor cortex activation improvement under stimulation with L-Dopa concerned both the movement preparation and execution but remained very localised to the contralateral motor cortex.

Aged↗

Does post-movement beta synchronization reflect an idling motor cortex?

After the completion of a voluntary movement, a synchronization of cortical beta rhythms is recorded over the contralateral central region, which is assumed to reflect the termination of the motor command. In order to test this hypothesis, we compared in eight healthy subjects the synchronization of EEG beta rhythms following active and passive index extension. The passive movement was also performed after deafferentation by ischaemic nerve block in three subjects. Beta synchronization was present in all subjects after both active and passive movements, and disappeared under ischaemia in all three subjects. Post-movement beta synchronization can not solely be explained by an idling motor cortex. It may also, at least in part, reflect a movement-related somatosensory processing.

Adult↗

Intermuscular coherence in Parkinson's disease: relationship to bradykinesia.

We hypothesised that bradykinesia may be partly due to the failure of the corticomuscular system to engage in high frequency oscillatory activity in Parkinson's disease (PD). In healthy subjects such oscillations are evident in coherence between active muscles at 15--30 Hz. We therefore investigated the effects of therapeutic stimulation of the basal ganglia on this coherence and related it to changes in bradykinesia in the contralateral arm. Increases in coherence at 15--30 Hz and improvements in bradykinesia upon stimulation were correlated (r = 0.564, p < 0.001). This suggests that the basal ganglia modulate oscillatory activity in the corticomuscular system and that impairment of the motor system's ability to engage in synchronised oscillations at high frequency may contribute to bradykinesia in PD.

Electric Stimulation Therapy↗

[Gait disorders in Parkinson disease. Neuroanatomic and physiologic organization of gait].

GAIT IS A VOLUNTARY, AUTOMATIC AND REFLEX RHYTHMIC ACTIVITY: It is generated by a central pattern generator identified from animal models. This spinal gait generator (SGG) is controlled by various parts of the central nervous system: the descending tracts and locomotor regions of the brainstem, the cerebellum, the basal ganglia, the motor and parietal cortex and the hippocampus. Kinesthetic inputs which project to the SGG and the cerebellum, play an important role in the production of postural reflex responses; vestibular and visual inputs mainly control balance. GAIT MAINLY DEPENDS ON THE RELATIONSHIP BETWEEN POSTURE BALANCE AND MOVEMENT: As concerns posture each segment is under the control of both peripheral and central nervous systems and is used as a system of reference to organize movements of adjacent segments. Balance is maintained by sensory inputs which provide corrective mechanisms: anticipatory postural responses, reflex postural responses and voluntary responses. DIFFERENT DESCRIPTIVE PARAMETERS MAY BE PROPOSED: Analysis of kinematic (displacement, speed and acceleration of segments) and kinetic parameters during the four successive stages of gait (posture, initiation, rhythmic gait and return to the initial posture) provides an understanding of neurological gait disorders. In particular the relationship between the center of pressure and the center of gravity is used to analyze infraclinical gait abnormalities. NEW AND SOPHISTICATED INVESTIGATIONS METHODS ARE AVAILABLE: The optoelectronic system provides a tridimensional analysis of movement and can be combined with forceplate and electromyographic recordings. These methods constitute an interesting contribution to the clinical analysis of gait. CLASSIFICATION: This is established according to clinical data and the positionment of the lesion among the structures of the nervous system. The physiopathological approach is then specified taking into account the lesions of the muscular, skeletal and nervous structures.

Brain↗

[Gait disorders in Parkinson disease. Clinical description, analysis of posture, initiation of stabilized gait].

A WELL INFORMED DESCRIPTION: The parkinsonian posture is generally described as a stooped one. At the beginning of the disease, the gait troubles remain moderate; gradually the gait is composed of small steps without a wide base; the patient tends to run after his centre of gravity by accelerating the step (festination phenomenon). Difficulties occurs for starting up (delay of gait initiation), for about-turn or for clearing obstacles. Kinetic jammings and standing around (freezing) can last several seconds and be responsible for falls. POSTURAL INSTABILITY, A MAJOR SYMPTOM IN PARKINSON'S DISEASE: This symptom is little improved by therapies and is responsible for serious disability. Postural instability induces a disequilibrium and is partially due to a simultaneous antagonist muscles contraction and to the impossibility of modifying postural responses to changing support conditions. The passive viscoelastic properties of muscles and tendons constitute a first line of defence against the disequilibrium and contribute to postural stability in the case of medium disturbances. Automatic and voluntary postural responses which come into play in the case of major disturbances can also be impaired (delay or defect of the responses). GAIT INITIATION FAILURE ARE FREQUENT: They result from an increase of the postural phase and a decrease of the propulsion forces, depending on a deficit of the postural anticipation mechanisms and also the sequential organization and the integration of two different motor programs, postural and locomotor. They can be controlled partially with sensory stimuli, notably visual inputs. DATA CONCERNING STABILIZED WALKING AND ITS PATHOPHYSIOLOGY REMAINS TO BE CLARIFIED: Spatial and temporal parameters are impaired: speed, step length and swing phase are reduced, while cadence increases to compensate these troubles. These modifications are the consequence of an incapacity to produce internal marks to generate regular steps. When the parkinsonian patient is supplied with external marks, these parameters can be normalized. From a pathophysiological point of view, gait disorders could result from defective central integration of proprioceptive information during movement within the basal ganglia, associated with a visual perceptive deficit linked with a retinal dopaminergic cells dysfunction and finally from an impairment of the proprioceptive feedback of the load receptors in the leg extensor muscles.

Antiparkinson Agents↗

[Gait disorders in Parkinson disease. Gait freezing and falls: therapeutic management].

GAIT ARRESTS: They affect the evolution of the disease. This freezing phenomenon which induces falls sometimes constitutes an initial sign. Like the gait initiation failure, freezing can be controlled by sensory stimulation, notably visual inputs, but also by more sustained attention. FALLS ARE MAINLY CONNECTED WITH BOTH POSTURAL INSTABILITY AND RIGIDITY: They are poorly influenced by dopaminergic therapies. The progressive decrease of step width represents a main factor in their occurrence. PRECOCITY OF GAIT DISORDERS IS UNUSUAL IN PARKINSON'S DISEASE: Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy and vascular parkinsonian syndrome must then be evoked. Their association with a cognitive impairment and abnormal sphincter behaviour infers a diagnosis of normal pressure hydrocephalus. GAIT IMPROVES WITH L-DOPA THERAPY: Speed, step length and duration of the swing phase are increased without change of cadence. Progressive loss of L-dopa efficiency on gait and postural stability contrasts with the persistent effect on tremor, rigidity and bradykinesia; a functional abnormality of nondopaminergic systems can explain these symptoms. In the following stages, gait troubles increased by motor fluctuations and abnormal involuntary movements are less controlled by L-dopa therapy. PHYSICAL THERAPY PLAYS A MAJOR ROLE IN THERAPEUTIC MANAGEMENT: An individual or collective rehabilitation project must be established according to the stage of evolution; the exercises aim to protect postural control and coordination. Visual or sound rhythmic inputs can be employed in the case of gait initiation failure. THE EFFECTS OF FUNCTIONAL NEUROSURGERY ARE IN THE COURSE OF EVALUATION: Thermolesion and chronic electrical stimulation of deep brain structures have opposite effects on gait troubles. Bilateral thalamotomy or pallidotomy are sometimes a source of disequilibrium. Chronic thalamic stimulation does not induce either benefits or adverse effects. On the other hand, stimulation of the internal pallidum improves gait kinematic parameters; improved postural adjustments have also been reported. The effect of subthalamic nucleus stimulation is comparable to that of L-dopa, however the long-term effect remains to be evaluated.

Accidental Falls↗

Genetic analysis of synphilin-1 in familial Parkinson's disease.

alpha-Synuclein is present in Lewy bodies of patients with both sporadic and familial Parkinson's disease. However, pathogenic mutations Ala30Pro and Ala53Thr in alpha-synuclein are rare causes of disease. Synphilin-1 has been demonstrated to associate with alpha-synuclein and promote the formation of cytosolic inclusions in vitro. Two-point genetic linkage analysis of a dinucleotide repeat within the synphilin-1 gene initially implicated this locus as a cause of Parkinson's disease in three of nine families. However, subsequent haplotype, sequencing, and association analyses in these three families and an independent case-control series suggest that variability within the locus does not confer susceptibility to Parkinson's disease.

Aged↗

Chronic bilateral pallidal stimulation and levodopa do not improve gait in the same way in Parkinson's disease: a study using a video motion analysis system.

Chronic bilateral internal globus pallidus (GPi) stimulation allows control of levodopa induced dyskinesias (LID) and motor symptoms in severe Parkinson's disease (PD). The effect on gait has not been clearly established. Different results have been reported, mostly consisting of clinical data. The aim of this study was to evaluate, by means of a video motion analysis system (optoelectronic VICON system), the influence of bilateral GPi stimulation on gait in PD. Five patients underwent bilateral GPi stimulation. The preoperative and postoperative (3 months after surgery) clinical gait disturbances (items 29 and 30 of the motor UPDRS), as well as spatial and temporal gait measurements (namely cadence, velocity, stride and step times, single and double limb support times, stride and step lengths) were analysed in off condition (the patient had received no treatment for 12 hours or merely the lowest dose of levodopa allowing him to walk for the gait analysis) and in the on drug condition (after administration of 200 mg of levodopa). The gait analysis was performed with the VICON system. In off condition, there was a statistically significant improvement after surgery for UPDRS III and gait (clinically assessed). In on drug condition, there was a significant improvement for LID whereas UPDRS III and clinical assessment of gait were unchanged. The VICON system also showed that surgery improved gait especially in off condition, but also in on drug condition. Our method allowed exact quantification of the influence of surgery on gait characteristics. As compared with levodopa treatment, the effect of stimulation seems to be different. Indeed, the results suggest only limited effects of pallidal stimulation on the control of stride length and rather point to compensatory additional mechanisms.

Aged↗

Influence of chronic bilateral stimulation of the subthalamic nucleus on cognitive function in Parkinson's disease.

BACKGROUND: The clinical efficacy of chronic deep brain stimulation in the treatment of parkinsonian patients with severe levodopa-related motor adverse effects has been repeatedly shown. Bilateral subthalamic nucleus (STN) stimulation has been shown to present an advantage over pallidal stimulation as it induces a higher antiakinetic effect and has positive effects on all parkinsonian symptoms. The morbidity of such surgery is usually considered to be very low. However, few studies have extensively examined the effects of chronic STN stimulation on cognitive function. OBJECTIVE: The aim of the present study was to assess the effects of chronic bilateral STN stimulation on performance in an extensive battery of neuropsychological tests, three months and one year after surgery. METHODS: Nine patients with Parkinson's disease were selected for STN electrodes implantation. They underwent a neuropsychological evaluation at one month before and at three months after surgery. Six of them were examined again at one year after surgery. RESULTS: Before surgery, no patient showed cognitive decline. At three months after surgery, no modification was observed for most tasks. The information processing speed tended to improve. There was a significant reduction of the performance in a delayed free recall test and a trend toward a significant reduction of categorial word fluency. At one year after surgery, most task measures did not change. Slight impairment was observed for tasks evaluating executive function. Examination of individual results showed that some patients (30% at 3 months after surgery) showed an overall cognitive decline. Behavioural changes were also observed in 4 patients with overall cognitive decline in one of them. CONCLUSION: In general, STN deep brain stimulation can be considered as a significant contribution to the treatment of severe Parkinson's disease However, in some patients it can induce overall cognitive decline or behavioural changes.

Cognition Disorders↗

No genetic association of the ubiquitin carboxy-terminal hydrolase-L1 gene S18Y polymorphism with familial Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder for which genetic susceptibility has been documented in sporadic and familial cases. Recently, a polymorphism located in exon 3 at codon 18 (S18Y) of the Ubiquitin Carboxy-terminal Hydrolase-L1 (UCH-L1) gene has been associated with the disease in 2 populations of German origin and also in a Japanese population. We tested the impact of this polymorphism in a French sample of familial PD patients (n = 114) and controls (n = 93). No association was observed, indicating that this polymorphism did not confer susceptibility for familial PD in our population, even among the youngest age of onset group. This observation suggests that the previous positive results obtained may reflect mechanisms restricted to the sporadic form of the disease or to a founder effect of the disease susceptibility.

Age of Onset↗

Memory and executive function in sporadic and familial Parkinson's disease.

Some studies have demonstrated that the motor symptomatology in sporadic and familial Parkinson's disease was identical. From a physiopathological point of view, and perhaps in the future from a therapeutic point of view, it seems important to determine whether sporadic and familial Parkinson's disease are also similar with regard to cognitive impairment. The aim of the present study was to assess cognitive functions in patients suffering from sporadic and familial Parkinson's disease. Executive functions and memory were investigated in particular. Two groups of 12 patients with Parkinson's disease (sporadic and familial) and 12 healthy controls performed a set of tasks known to evaluate different aspects of executive function and memory. One-way analysis of variance tested for significant group effects, and when justified, post hoc analysis was performed. Cognitive impairment was different in sporadic and familial forms of Parkinson's disease. Indeed, although executive function was impaired in both groups of patients, deficits in tests of explicit memory recall were only observed in patients with sporadic Parkinson's disease. Although the impairment observed in both groups of patients suggests a disruption of the striatoprefrontal circuits, this disruption seems to be quantitatively more important and more widespread in the sporadic patients than in the familial ones. In both patient groups, the deficits probably result from dopaminergic and nondopaminergic deprivation and a greater participation of nondopaminergic factors in patients with sporadic Parkinson's disease could be suggested. In this group, a xenobiotic could be responsible for an acquired metabolic defect involving more widespread structures of the striatoprefrontal circuits, leading to disruption of nondopaminergic loops. Cholinergic deprivation is considered in particular.

Adult↗