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Sainte-Foy-lès-Lyon, France

Maarrawi J.,French Institute of Health and Medical Research | Maarrawi J.,Damascus University | Peyron R.,French Institute of Health and Medical Research | Mertens P.,French Institute of Health and Medical Research | And 5 more authors.
Pain | Year: 2013

The clinical effects of motor cortex stimulation (MCS) for neuropathic pain (NP) is thought to be mediated primarily by the secretion of endogenous opioids in humans and in animal models. Because opioid receptor density is itself decreased in patients with NP, we investigated whether the magnitude and distribution of the remaining opioid receptors in patients with NP could be biological predictors of the pain-relieving effects of MCS. Using 11C-diprenorphine positron emission tomography scans, opioid receptor availability was assessed in 15 patients suffering refractory NP, who subsequently received chronically implanted MCS. All patients underwent 2 preoperative baseline scans at 2-wk intervals and were clinically assessed after 7 mo of chronic MCS. The levels of preoperative opioid-binding in the insula, thalamus, periaqueductal gray, anterior cingulate, and orbitofrontal cortex were significantly and positively correlated with postoperative pain relief at 7 mo. Patients with receptor density values below the lower limits in age-matched controls in the thalamus, periaqueductal gray and contralateral insula were the least likely to benefit from MCS. Opioid-receptor availability as shown in preoperative positron emission tomography scans appears to be related to the efficacy of MCS in NP and may help clinicians to select the candidates most likely to benefit from this procedure. © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Source


Bor J.,University of Lyon | Brunelin J.,University of Lyon | d'Amato T.,University of Lyon | Costes N.,CERMEP Imagerie du Vivant | And 3 more authors.
Psychiatry Research - Neuroimaging | Year: 2011

Cognitive remediation therapy (CRT) is a non biological treatment that aims to correct cognitive deficits through repeated exercises. Its efficacy in patients with schizophrenia is well recognized, but little is known about its effect on cerebral activity. Our aim was to explore the impact of CRT on cerebral activation using functional magnetic resonance imaging (fMRI) in patients with schizophrenia. Seventeen patients and 15 healthy volunteers were recruited. Patients were divided into two groups: one group received CRT with Rehacom® software (n= 8), while a control group of patients (non-CRT group) received no additional treatment (n= 9). The three groups underwent two fMRI sessions with an interval of 3. months: they had to perform a verbal and a spatial n-back task at the same performance level. Patients were additionally clinically and cognitively assessed before and after the study. After CRT, the CRT group exhibited brain over-activations in the left inferior/middle frontal gyrus, cingulate gyrus and inferior parietal lobule for the spatial task. Similar but nonsignificant over-activations were observed in the same brain regions for the verbal task. Moreover, CRT patients significantly improved their behavioural performance in attention and reasoning capacities. We conclude that CRT leads to measurable physiological adaptation associated with improved cognitive ability.Trial name: Cognitive Remediation Theraphy and Schizophrenia.http://clinicaltrials.gov/ct2/show/NCT01078129.Registration number: NCT01078129. © 2010 Elsevier Ireland Ltd. Source


Lemoine L.,University of Lyon | Verdurand M.,University of Lyon | Vacher B.,Pierre Fabre | Blanc E.,Pierre Fabre | And 3 more authors.
European Journal of Nuclear Medicine and Molecular Imaging | Year: 2010

Purpose: The serotonin-1A (5-HT1A) receptor is implicated in the pathophysiology of major neuropsychiatric disorders. Thus, the functional imaging of 5-HT1A receptors by positron emission tomography (PET) may contribute to the understanding of its role in those pathologies and their therapeutics. These receptors exist in high- and low-affinity states and it is proposed that agonists bind preferentially to the high-affinity state of the receptor and therefore could provide a measure of the functional 5-HT 1A receptors. Since all clinical PET 5-HT1A radiopharmaceuticals are antagonists, it is of great interest to develop a 18F labelled agonist. Methods: F15599 (3-chloro-4-fluorophenyl-(4- fluoro-4{[(5-methyl-pyrimidin-2-ylmethyl)-amino]-methyl}-piperidin-1-yl) -methanone) is a novel ligand with high affinity and selectivity for 5-HT 1A receptors and is currently tested as an antidepressant. In pharmacological tests in rat, it exhibits preferential agonist activity at post-synaptic 5-HT1A receptors in cortical brain regions. Here, its nitro-precursor was synthesised and radiolabelled via a fluoronucleophilic substitution. Radiopharmacological evaluations included in vitro and ex vivo autoradiography in rat brain and PET scans on rats and cats. Results were compared with simultaneous studies using [18F]MPPF, a validated 5-HT1A antagonist radiopharmaceutical. Results: The chemical and radiochemical purities of [18F]F15599 were >98%. In vitro [ 18F]F15599 binding was consistent with the known 5-HT1A receptors distribution (hippocampus, dorsal raphe nucleus, and notably cortical areas) and addition of Gpp(NH)p inhibited [18F]F15599 binding, consistent with a specific binding to G protein-coupled receptors. In vitro binding of [18F]F15599 was blocked by WAY100635 and 8-OH-DPAT, respectively, prototypical 5-HT1A antagonist and agonist. The ex vivo and in vivo studies demonstrated that the radiotracer readily entered the rat and the cat brain and generated few brain radioactive metabolites. Remarkably, in microPET studies, [18F]F15599 notably displayed a pattern of brain labelling that did not correlate with in vitro observations. Thus, in cat, the highest binding was observed in dorsal raphe and cingulate cortex with little binding in other cortical regions and none in hippocampus. In vivo binding was abolished by WAY100635, indicating specific labelling of 5-HT1A receptors. Conclusion: [18F]F15599 is a radiofluorinated agonist presenting interesting characteristics for probing in vitro and in vivo the high-affinity states of the 5-HT1A receptors. Its differential labelling of 5-HT1A receptors in vitro and in vivo may result from its reported preferential interaction with receptors coupled to specific G-protein subtypes. © 2009 Springer-Verlag. Source


Brunelin J.,University of Lyon | Brunelin J.,South Limburg Mental Health Research and Teaching Network | d'Amato T.,University of Lyon | Van Os J.,South Limburg Mental Health Research and Teaching Network | And 4 more authors.
Psychiatry Research - Neuroimaging | Year: 2010

A genetic alteration in sensitivity to stress, mediated by mesolimbic hyperdopaminergia, is thought to play a role in the onset, exacerbation and relapse of schizophrenia. Dopamine sensitivity to stress was tested in individuals at higher than average genetic risk for schizophrenia (siblings of patients). Using a PET paradigm of [11C]raclopride in a bolus plus constant infusion tracer injection, the central DA response to acute metabolic stress (bolus of 2-Deoxy-d-Glucose, 40 mg/kg) in unaffected siblings of patients with schizophrenia (n = 8) and healthy controls (n = 10) was measured by BPND of [11C]raclopride before and after the 2DG challenge. After metabolic stress, controls but not siblings displayed a significant decrease in BPND of [11C]raclopride in the striatum; no such differences were apparent in the ventral striatum. Siblings but not controls displayed significant asymmetry (L > R) in the stress-induced DA release, especially in ventral striatum, which correlated strongly with psychometric measures of psychosis liability. The results suggest that asymmetry in the mesolimbic DA response to stress is associated with genetic risk for schizophrenia, possibly reflecting the functional consequences of structural disconnectivity underlying psychotic symptoms. © 2009 Elsevier Ireland Ltd. All rights reserved. Source


Eichenlaub J.-B.,Lyon Neuroscience Research Center | Eichenlaub J.-B.,University Claude Bernard Lyon 1 | Nicolas A.,Center Hospitalier le Vinatier | Daltrozzo J.,Lyon Neuroscience Research Center | And 5 more authors.
Neuropsychopharmacology | Year: 2014

Dreaming is still poorly understood. Notably, its cerebral underpinning remains unclear. Neuropsychological studies have shown that lesions in the temporoparietal junction (TPJ) and/or the white matter of the medial prefrontal cortex (MPFC) lead to the global cessation of dream reports, suggesting that these regions of the default mode network have key roles in the dreaming process (forebrain 'dream-on' hypothesis). To test this hypothesis, we measured regional cerebral blood flow (rCBF) using 15 OH 2 O positron emission tomography in healthy subjects with high and low dream recall frequencies (DRFs) during wakefulness (rest) and sleep (rapid eye movement (REM) sleep, N2, and N3). Compared with Low recallers (0.5±0.3 dream recall per week in average), High recallers (5.2±1.4) showed higher rCBF in the TPJ during REM sleep, N3, and wakefulness, and in the MPFC during REM sleep and wakefulness. We demonstrate that the resting states of High recallers and Low recallers differ during sleep and wakefulness. It coheres with previous ERP results and confirms that a high/low DRF is associated with a specific functional organization of the brain. These results support the forebrain 'dream-on' hypothesis and suggest that TPJ and MPFC are not only involved in dream recall during wakefulness but also have a role in dreaming during sleep (production and/or encoding). Increased activity in the TPJ and MPFC might promote the mental imagery and/or memory encoding of dreams. Notably, increased activity in TPJ might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, facilitating the encoding of the dreams in memory. © 2014 American College of Neuropsychopharmacology. Source

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