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Articles by L Tremblay
Total Records ( 2 ) for L Tremblay
  S Thobois , C Ardouin , E Lhommee , H Klinger , C Lagrange , J Xie , V Fraix , M. C Coelho Braga , R Hassani , A Kistner , A Juphard , E Seigneuret , S Chabardes , P Mertens , G Polo , A Reilhac , N Costes , D LeBars , M Savasta , L Tremblay , J. L Quesada , J. L Bosson , A. L Benabid , E Broussolle , P Pollak and P. Krack

Apathy has been reported to occur after subthalamic nucleus stimulation, a treatment of motor complications in advanced Parkinson’s disease. We carried out a prospective study of the occurrence of apathy and associated symptoms, predictors and mechanisms in the year following subthalamic stimulation. Dopamine agonist drugs were discontinued immediately after surgery and levodopa was markedly reduced within 2 weeks. Apathy and depression were assessed monthly, using the Starkstein apathy scale and the Beck Depression Inventory. Dopamine agonists were re-introduced if patients developed apathy or depression. Preoperative non-motor fluctuations were evaluated using the Ardouin Scale. Depression, apathy and anxiety were evaluated both on and off levodopa. Analysis of predictors of apathy was performed using a Cox proportional hazard model. Twelve patients who developed apathy and a control group of 13 patients who did not underwent [11C]-raclopride positron emission tomography scanning before and after oral intake of methylphenidate. In 63 patients with Parkinson’s disease treated with subthalamic stimulation, dopaminergic treatment was decreased by 82% after surgery. Apathy occurred after a mean of 4.7 (3.3–8.2) months in 34 patients and was reversible in half of these by the 12-month follow-up. Seventeen patients developed transient depression after 5.7 (4.7–9.3) months and these fell into the apathy group with one single exception. At baseline, fluctuations in depression, apathy and anxiety scores were greater in the group with apathy. Fluctuations in apathy, depression and anxiety ratings during a baseline levodopa challenge were also significant predictors of postoperative apathy in univariate analysis, but not motor and cognitive states or the level of reduction of dopaminergic medication. The multivariate model identified non-motor fluctuations in everyday life and anxiety score during the baseline levodopa challenge as two independent significant predictors of postoperative apathy. Without methylphenidate, [11C]-raclopride binding potential values were greater in apathetic patients bilaterally in the orbitofrontal, dorsolateral prefrontal, posterior cingulate and temporal cortices, left striatum and right amygdala, reflecting greater dopamine D2/D3 receptor density and/or reduced synaptic dopamine level in these areas. The variations of [11C]-raclopride binding potential values induced by methylphenidate were greater in non-apathetic patients in the left orbitofrontal cortex, dorsolateral prefrontal cortex, thalamus and internal globus pallidus and bilaterally in the anterior and posterior cingulate cortices, consistent with a more important capacity to release dopamine. Non-motor fluctuations are related to mesolimbic dopaminergic denervation. Apathy, depression and anxiety can occur after surgery as a delayed dopamine withdrawal syndrome. A varying extent of mesolimbic dopaminergic denervation and differences in dopaminergic treatment largely determine mood, anxiety and motivation in patients with Parkinson’s disease, contributing to different non-motor phenotypes.

  Y Worbe , E Gerardin , A Hartmann , R Valabregue , M Chupin , L Tremblay , M Vidailhet , O Colliot and S. Lehericy

Gilles de la Tourette syndrome is a childhood-onset neurodevelopmental disorder characterized by tics that are often associated with psychiatric co-morbidities. The clinical heterogeneity of Gilles de la Tourette syndrome has been attributed to the disturbance of functionally distinct cortico-striato-thalamo-cortical circuits, but this remains to be demonstrated. The aim of this study was to determine the structural correlates of the diversity of symptoms observed in Gilles de la Tourette syndrome. We examined 60 adult patients and 30 age- and gender-matched control subjects using cortical thickness measurement and 3 T high-resolution T1-weighted images. Patients were divided into three clinical subgroups: (i) simple tics; (ii) simple and complex tics and (iii) tics with associated obsessive–compulsive disorders. Patients with Gilles de la Tourette syndrome had reduced cortical thickness in motor, premotor, prefrontal and lateral orbito-frontal cortical areas. The severity of tics was assessed using the Yale Global Tic Severity Scale and correlated negatively with cortical thinning in these regions, as well as in parietal and temporal cortices. The pattern of cortical thinning differed among the clinical subgroups of patients. In patients with simple tics, cortical thinning was mostly found in primary motor regions. In patients with simple and complex tics, thinning extended into larger premotor, prefrontal and parietal regions. In patients with associated obsessive–compulsive disorders, there was a trend for reduced cortical thickness in the anterior cingulate cortex and hippocampal morphology was altered. In this clinical subgroup, scores on the Yale–Brown Obsessive–Compulsive Scale correlated negatively with cortical thickness in the anterior cingulate cortex and positively in medial premotor regions. These data support the hypothesis that different symptom dimensions in Gilles de la Tourette syndrome are associated with dysfunction of distinct cortical areas and have clear implications for the current neuroanatomical model of this syndrome.

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