No description available.

Beaucoup de patients atteints de la maladie de Parkinson (MP) peuvent souffrir de troubles cognitifs dès les étapes initiales de la maladie et jusqu’à 80% d’entre eux vont développer une démence. Des altérations fonctionnelles au niveau du cortex préfrontal dorsolatéral (CPFDL), possiblement en relation avec le noyau caudé, seraient à l’origine de certains de ces déficits cognitifs. Des résultats antérieurs de notre groupe ont montré une augmentation de l’activité et de la connectivité dans la boucle cortico-striatale cognitive suite à la stimulation magnétique transcrânienne (SMT) utilisant des paramètres « theta burst » intermittent (iTBS) sur le CPFDL gauche. Pour cette étude, 24 patients atteints de la MP avec des troubles cognitifs ont été séparées en 2 groupes : le groupe iTBS active (N=15) et le groupe sham (stimulation simulée, N=9). Une batterie neuropsychologique détaillée évaluant cinq domaines cognitifs (attention, fonctions exécutives, langage, mémoire et habiletés visuo-spatiales) a été administrée lors des jours 1, 8, 17 et 37. Le protocole iTBS a été appliqué sur le CPFDL gauche durant les jours 2, 4 et 7. Les scores z ont été calculés pour chaque domaine cognitif et pour la cognition globale. Les résultats ont montré une augmentation significative de la cognition globale jusqu’à 10 jours suivant l’iTBS active, particulièrement au niveau de l’attention, des fonctions exécutives et des habiletés visuo-spatiales. Cet effet sur la cognition globale n’est pas répliqué dans le groupe sham. Ces résultats suggèrent donc que l’iTBS peut moduler la performance cognitive chez les patients atteints de MP avec des déficits cognitifs. / Cognitive impairment affects many patients with Parkinson’s disease (PD) in the early phase of the disease and up to 80% of them will eventually develop dementia. Many studies suggests that these cognitive deficits are mediated by functional alterations in the dorsolateral prefrontal cortex (DLPFC), possibly in relation with the caudate nucleus. Previous results from our group showed an increase in activity and connectivity within the cognitive cortico-striatal loop when applying transcranial magnetic stimulation (TMS) using intermittent « theta burst » (iTBS) parameters over left DLPFC. For this study, 24 idiopathic PD patients with cognitive impairment were recruited and divided into two groups : active iTBS group (N=15) and sham group (simulated stimulation, N=9). Detailed neuropsychological assessment of five cognitive domains (attention, executive functions, language, memory, visuospatial abilities) was performed on day 1, 8, 17 and 37. iTBS protocol over left DLPFC was performed on day 2, 4 and 7. Z scores were calculated for each domain and for the overall cognition performance. Our results showed a significant increase in overall cognition up to 10 days after receiving active iTBS, improving mainly attention, executive functions and visuospatial abilities. This effect was not replicated in the sham group. Therefore, our results suggest that iTBS can modulate cognitive performance in PD patients with cognitive deficits.

No description available.

Introduction: Memory is a complex cognitive process formerly linked to mechanisms of brain plasticity that can be estimated in the left dorsolateral prefrontal cortex (DLPFC) using transcranial magnetic stimulation and electroencephalography (TMS-EEG). Also, cortical thickness in the DLPFC may be a potential proxy measure of brain plasticity as previous literature reports a link between better memory and thicker cortex. However, the link between brain plasticity and memory performance as well as DLPFC thickness remains to be clarified. Methods: Intermittent theta burst stimulation (iTBS) probed plasticity-like mechanisms in the left DLPFC in 17 cognitively healthy participants. TMS-EEG recordings were performed before and after sham and active iTBS to quantify plasticity via transcranial magnetic stimulation-evoked potentials (TEPs). Composite memory scores for each domain (verbal episodic, visual episodic and working memory) were obtained using the Cambridge Neuropsychological Test Automated Battery. Anatomical T1 images were acquired by magnetic resonance imaging and processed by open-source software (CIVET) and the Automated Anatomical Labeling atlas to extract cortical thickness of the DLPFC. All statistical analyses (linear mixed model, Tukey's post hoc test and Pearson's correlations) were completed in R Studio. Results: iTBS resulted in increased TEP amplitude P30 (F= 5.239, p = 0.029), as shown by a significant interaction between condition (iTBS, sham) and time (pre- and post-condition). Specifically, Tukey's post hoc test revealed that the P30 increase was near trending significant post-iTBS compared to pre-iTBS for the active condition (p = 0.166) but not for the sham condition (p = 0.294). A trending significant relationship was observed between the magnitude of P30 change post-iTBS and thicker left DLPFC (r = 0.488; p = 0.108). Lastly, no significant relationships between P30 change and memory performance were observed. Conclusion: These preliminary findings suggest there could be a relationship between increased capacity for brain plasticity and a thicker left DLPFC. To further investigate these relationships, we plan to recruit additional cognitively healthy participants. Our preliminary findings support the foundation for future clinical studies in which DLPFC thickness could be explored as a predictive factor for response to plasticity-targeting iTBS treatment.