[How to improve social and professional reinsertion of patients with neurodiabilities ? Practical indications for the general practitioner]. / Comment faciliter la réinsertion socioprofessionnelle du patient neurolésé ? Outils pour le praticien.

One part of the population of neurolesioned patients is the transition of young patients with neurodisabilities to adult life. To guarantee favourable social and professional reinsertion is a major challenge, requiring inter-professional care. For this reason, in 2006 the CHUV, Lausanne created a transition-consultation framework with neuro-paediatricians and adult neurologists specialised in neuro-rehabilitation linked to a Swiss pilot social and professional reinsertion project collaborating with the invalidity insurance. As a model of the follow up of neurolesioned patients, this article reports the results of the reinsertion project that aims to bring awareness to the general practitioner of an inter-disciplinary care method adaptable to individuals. The holistic service saves time and improves the rate of successful reinsertion of young adults into social and professional life.

Les jeunes en transition de l'enfance à l'âge adulte présentant une maladie neurodéveloppementale sont une population spécialement vulnérable. Le suivi de leurs problèmes de santé et leur insertion socioprofessionnelle représentent un véritable défi. Au CHUV, à Lausanne, une consultation de transition entre les neurorééducateurs pédiatriques et adultes a été créée en 2006 ainsi qu'un projet pilote suisse de réinsertion socioprofessionnelle en collaboration avec l'Office de l'assurance invalidité pour le canton de Vaud. Le résultat de ce projet pilote, qui peut être utilisé comme modèle pour tous les patients neurolésés, est rapporté ici avec comme objectif d'informer le médecin traitant et de lui permettre d'utiliser les outils de cette prestation holistique afin d'optimiser la durée et la qualité de la réinsertion.

Effect of repetitive arm cycling following botulinum toxin injection for poststroke spasticity: evidence from FMRI.

BACKGROUND AND OBJECTIVE: Investigations were performed to establish if repetitive arm cycling training enhances the antispastic effect of intramuscular botulinum toxin (BTX) injections in postischemic spastic hemiparesis. Effects on cerebral activation were evaluated by functional magnetic resonance imaging (fMRI). METHODS: Eight chronic spastic hemisyndrome patients (49 ± 10 years) after middle cerebral artery infarction (5.5 ± 2.7 years) were investigated. BTX was injected into the affected arm twice, 6 months apart. Spasticity was assessed using the Ashworth Scale and range of motion before and 3 months after BTX injections. Images were analyzed using Brain Voyager QX 1.8, and fMRI signal changes were corrected for multiple comparisons. RESULTS: During passive movements of affected and nonaffected hands, fMRI activity was increased bilaterally in the sensorimotor cortex (MISI), secondary somatosensory areas (SII), and supplementary motor area predominantly in the contralesional hemisphere, compared with the rest. Following repetitive arm cycling, fMRI activity increased further in MISI of the lesioned hemisphere and SII of the contralesional hemisphere. For patients with residual motor activity, treatment-related fMRI activity increases were associated with reduced spasticity; in completely plegic patients, there was no fMRI activity change in SII but increased spasticity after training. CONCLUSION: Increased activity in SII of the contralesional hemisphere and in MISI of the lesioned hemisphere reflect a treatment-induced effect in the paretic arm. It is hypothesized that the increased BOLD activity results from increased afferent information related to the antispastic BTX effect reinforced by training.

Delta-9-tetrahydrocannabinol accumulation, metabolism and cell-type-specific adverse effects in aggregating brain cell cultures.

Despite the widespread use of Cannabis as recreational drug or as medicine, little is known about its toxicity. The accumulation, metabolism and toxicity of THC were analyzed 10 days after a single treatment, and after repeated exposures during 10 days. Mixed-cell aggregate cultures of fetal rat telencephalon were used as in vitro model, as well as aggregates enriched either in neurons or in glial cells. It was found that THC accumulated preferentially in neurons, and that glia-neuron interactions decreased THC accumulation. The quantification of 11-OH-THC and of THC-COOH showed that brain aggregates were capable of THC metabolism. No cell-type difference was found for the metabolite 11-OH-THC, whereas the THC-COOH content was higher in mixed-cell cultures. No cell death was found at THC concentrations of 2 microM in single treatment and of 1 microM and 2 microM in repeated treatments. Neurons, and particularly GABAergic neurons, were most sensitive to THC. Only the GABAergic marker was affected after the single treatment, whereas the GABAergic, cholinergic and astrocytic markers were decreased after the repeated treatments. JWH 015, a CB2 receptor agonist, showed effects similar to THC, whereas ACEA, a CB1 receptor agonist, had no effect. The expression of the cytokine IL-6 was upregulated 48 h after the single treatment with 5 microM of THC or JWH 015, whereas the expression of TNF-alpha remained unchanged. These results suggest that the adverse effects of THC were related either to THC accumulation or to cannabinoid receptor activation and associated with IL-6 upregulation.