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International audience; Apathy occurs in approximately one third of people after stroke. Despite its frequency and functional consequences, the determinants of apathy have only been partially defined. The major difficulty lies in disentangling the reduction in activity due to apathy itself from those secondary to comorbidities, such as depression, sensorimotor deficits, and cognitive impairment. Here, we aimed to examine the prevalence of apathy, identify confounding sources of hypoactivity, and define its neuroimaging determinants using multivariate voxel lesion symptom-mapping (mVLSM) analyses. We assessed apathy in a subgroup (n = 325, mean age: 63.8 ± 10.5 years, 91.1% ischemic stroke) of the GRECogVASC cohort using the validated Behavioral Dysexecutive Syndrome Inventory, interpreted using GREFEX criteria, as well as confounding factors (depression, anxiety, severity of the neurological deficit, and gait disorders). mVLSM analysis was used to define neuroimaging determinants and was repeated after controlling for confounding factors. Apathy was present for 120 patients (36.9%, 95% CI: 31.7-42.2). Stepwise linear regression identified three factors associated with apathy: depressive symptoms (R2 = .3, p = .0001), cognitive impairment (R2 = .015, p = .02), and neurological deficit (R2 = .110, p = .0001). Accordingly, only 9 (7.5%) patients had apathy without a confounding factor, i.e., isolated apathy. In conventional VLSM analysis, apathy was associated with a large number of subcortical lesions that were no longer considered after controlling for confounding factors. Strategic site analysis identified five regions associated with isolated apathy: the F3 orbitalis pars, left amygdala, left thalamus, left pallidum, and mesencephalon. mVLSM analysis identified four strategic sites associated with apathy: the right corticospinal tract (R2 = .11; p = .0001), left frontostriatal tract (R2 = .11; p = .0001), left thalamus (R2 = .04; p = .0001), and left amygdala (R2 = .01; p = .013). These regions remained significant after controlling for confounding factors but explained a lower amount of variance. These findings indicate that poststroke apathy is more strongly associated with depression, neurological deficit, and cognitive impairment than with stroke lesions locations, at least using VLSM analysis.

Although action slowing is the main cognitive impairment in stroke survivors, its mechanisms and determinants are still poorly understood. The objectives of the present study were to determine the mechanisms of post-stroke action slowing (using validated, highly specific simple reaction time (SRT) and tapping tests) and identify its imaging determinants (using multivariate lesion-symptom mapping (mLSM)).Action speed in the GRECogVASC cohort was assessed using finger tapping and SRT tests performed with both hands and analyzed using previously validated indices. Imaging determinants were identified using validated mLSM analyses and disconnection analysis and compared to those of an fMRI activation meta-analytic database.Both the tapping time and SRT were 10.7% slower for the 394 patients (p = 0.0001) than for the 786 controls, without a group × test interaction (p = 0.2). The intra-individual distribution curve was characterized by a rightward shift with an unaltered attentional peak. The mLSM analyses showed tapping to be associated with lesions in the frontostriatal tract (p = 0.0007). The SRT was associated with lesions in the frontostriatal tract (p = 0.04) and the orbital part of F3 (p = 0.0001). The SRT-tapping index was associated with lesions in the orbital part of F3 (p = 0.0001). All lesions were located in the right hemisphere only and were responsible for the disconnection of several structures involved in motor preparation, initiation, and speed. A comparison with fMRI activation meta-analytic data highlighted mostly the same regions, including the orbital part of F3, the ventral and dorsal parts of F1, and the premotor and cingulate regions in the right hemisphere.Our results confirm the marked impairment of action speed in stroke and show that the primary mechanism is motor slowing and that it is related to lesions in the right frontostriatal tract. A deficit in sustained alertness accounted for action slowing in the subgroup with lesions in the right orbital part of F3. Our SRT and mLSM results were in accordance with the fMRI activation data. Thus, stroke induces slowing in the broad network associated with SRT tasks by disrupting the frontostriatal tract and, to a lesser extent, other sites involved in attention.

Action slowing is frequently observed in multiple sclerosis (MS) patients. Several factors may account for response slowing: motor, perceptual, cognitive deficits, global mental slowing. Our objective was to examine mechanisms accounting for action slowing in MS patients.Twenty MS patients, free of visual impairment and of upper limbs sensory-motor deficit underwent previously validated reaction time (RT) tests using visual stimuli. Three tasks were used: (1) motor tapping, (2) simple reaction time (SRT) in a simple and dual task condition, and (3) choice RT (CRT) with varying response probabilities. Results were compared to those of 20 healthy matched subjects.MS patients had: (1) lower motor tapping frequency (p=0.02); (2) SRT lengthening (p=0.001) related to a lower proportion of fast responses (p=0.001) indicating attentional deficit whereas perceptuomotor index was spared (p=0.5), without higher sensitivity to dual task (p=0.9); and (3) CRT lengthening (p=0.001) with spared decision time (p=0.7).This study showed that action slowing of MS patient is mainly related to (1) attentional deficit resulting in inability to maintain high level of rapid actions, and (2) subtle motor slowing even in patients without motor deficit on clinical examination, whereas (3) divided attention and decisional process are preserved.

Introduction La dichotomisation manuelle des performances (normal vs pathologique), en fonction des criteres âge et de niveau socioculturel, d’un bilan neuropsychologique est couteuse en temps au regard des nombreux scores. Objectifs L’objectif du travail est de presenter un outil d’assistance informatise, « AMIENSCOG » et de montrer son interet lors de l’evaluation neuropsychologique et en particulier le gain de temps obtenu. Methodes L’interet de cet outil sera illustre en montrant qu’il permet de : – realiser automatiquement la dichotomisation des scores aux tests selon les donnees normatives ; – sauvegarder les donnees, en permettant de les consulter ou les modifier ; – d’exporter les scores et leur interpretation dichotomisee vers une base de donnees. Des analyses de comparaisons des temps de saisie et d’interpretation des scores aux bilans realises manuellement et avec « AMIENSCOG » ont ete effectuees. Resultats Durant la periode de 2008 a 2013, 4473 bilans ont ete effectues totalisant plus de 122000 scores qui ont ete rentres dans « AMIENSCOG » et automatiquement interpretes en normal vs pathologique. Les resultats de la comparaison entre les temps de saisie et l’interpretation des scores, montrent des temps pour « AMIENSCOG » (m = 284 ± 48 s) inferieurs ( p = 0,001) a ceux des bilans realises manuellement ( m = 284 ± 128 s). Discussion Ces resultats montrent que « AMIENSCOG » offre un gain de temps significatif sur la saisie et l’interpretation des scores mais aussi grâce a l’export automatique sur Excel. Il facilite et fiabilise le recueil et l’interpretation des scores automatiquement dichotomises en normal vs pathologique, en produisant une version papier synthetique regroupant les donnees cliniques et les scores en fonction des principales fonctions cognitive. Conclusion « AMIENSCOG » offre une aide precieuse au clinicien et chercheur en permettant un acces plus facile, plus rapide et plus fiable aux donnees neuropsychologiques disponibles avec un export possible vers une base de donnee. Informations complementaires Demonstration en direct possible du logiciel.