2011 |
Gillette-Guyonnet S.; Andrieu S.; Nourhashemi F.; Gardette V.; Coley N.; Cantet C.; Gauthier S.; Ousset P.J.; Vellas B.; REAL.FR study group Long-term progression of Alzheimer’s disease in patients under antidementia drugs. Article de journal Alzheimer's & Dementia, 7 (6), p. 579–592, 2011. @article{Gillette-Guyonnet2011, title = {Long-term progression of Alzheimer’s disease in patients under antidementia drugs.}, author = {Gillette-Guyonnet S. and Andrieu S. and Nourhashemi F. and Gardette V. and Coley N. and Cantet C. and Gauthier S. and Ousset P.J. and Vellas B. and REAL.FR study group}, doi = {10.1016/j.jalz.2011.02.009}, year = {2011}, date = {2011-11-01}, journal = {Alzheimer's & Dementia}, volume = {7}, number = {6}, pages = {579–592}, abstract = {BACKGROUND Patients with Alzheimer’s disease (AD), even in the presence of symptomatic relief from medical intervention, face a persistent worsening of cognitive decline and performance in activities of daily living. Data regarding the long-term disease progression outside of therapeutic trials are lacking. We examined the effects of standard of care for AD patients on the prognosis of the disease in a real-life study over a 4-year period. METHODS A total of 686 patients with mild-moderate AD were enrolled in 16 memory clinics (REseau sur la maladie d’ Alzheimer FRançais [REAL.FR] cohort) and followed up twice annually with tools used in therapeutic trials (Mini-Mental Status Examination, Alzheimer Disease Assessment Scale-cognitive subscale [ADAS-cog]: cognitive function, Clinical Dementia Rating: dementia severity, Activity of Daily Living [ADL]: incapacities, NeuroPsychiatric Inventory: neuropsychiatric symptom). RESULTS More than 90% of the patients used AD-specific medication over 4 years. Patients lost on average 2.4 points per year on the Mini-Mental Status Examination and gained 4.5 points on the ADAS-cog. ADL and NeuroPsychiatric Inventory scores became significantly worse over time. Incidence of incapacities for ADL and worsening of neuropsychiatric symptoms were 52.5 (95% confidence interval [CI]: 47.7-57.4) and 51.1 (95% CI: 46.2-56.1), respectively. Rates of mortality and institutionalization were 7.4 (95% CI: 6.2-8.5) and 13.4 (95% CI: 11.7-15.1). In all, 17% of patients in mild stage at baseline (Clinical Dementia Rating = 0.5) did not experience a major event (functional disabilities, neuropsychiatric symptoms, or death) over a 4-year period. CONCLUSIONS As compared with previous surveys, the current study shows slower rates of decline in AD patients. The present data also underline the high level of variability of disease progression among AD patients. Outcome measures commonly used in clinical trials will need to take into account the recent changes in the prognosis of the disease.}, keywords = {}, pubstate = {published}, tppubtype = {article} } BACKGROUND Patients with Alzheimer’s disease (AD), even in the presence of symptomatic relief from medical intervention, face a persistent worsening of cognitive decline and performance in activities of daily living. Data regarding the long-term disease progression outside of therapeutic trials are lacking. We examined the effects of standard of care for AD patients on the prognosis of the disease in a real-life study over a 4-year period. METHODS A total of 686 patients with mild-moderate AD were enrolled in 16 memory clinics (REseau sur la maladie d’ Alzheimer FRançais [REAL.FR] cohort) and followed up twice annually with tools used in therapeutic trials (Mini-Mental Status Examination, Alzheimer Disease Assessment Scale-cognitive subscale [ADAS-cog]: cognitive function, Clinical Dementia Rating: dementia severity, Activity of Daily Living [ADL]: incapacities, NeuroPsychiatric Inventory: neuropsychiatric symptom). RESULTS More than 90% of the patients used AD-specific medication over 4 years. Patients lost on average 2.4 points per year on the Mini-Mental Status Examination and gained 4.5 points on the ADAS-cog. ADL and NeuroPsychiatric Inventory scores became significantly worse over time. Incidence of incapacities for ADL and worsening of neuropsychiatric symptoms were 52.5 (95% confidence interval [CI]: 47.7-57.4) and 51.1 (95% CI: 46.2-56.1), respectively. Rates of mortality and institutionalization were 7.4 (95% CI: 6.2-8.5) and 13.4 (95% CI: 11.7-15.1). In all, 17% of patients in mild stage at baseline (Clinical Dementia Rating = 0.5) did not experience a major event (functional disabilities, neuropsychiatric symptoms, or death) over a 4-year period. CONCLUSIONS As compared with previous surveys, the current study shows slower rates of decline in AD patients. The present data also underline the high level of variability of disease progression among AD patients. Outcome measures commonly used in clinical trials will need to take into account the recent changes in the prognosis of the disease. |
De Paula A.M.; Michel B.F.; Dickson D.W.; Wszolek Z.K.; Pellissier J-F. Sporadic diffuse leucoencephalopathy with axonal spheroids: report of a profuse and rapid cortical-spinal degeneration. Article de journal Neurological Sciences, 33 (4), p. 905-909, 2011. @article{DePaula2011, title = {Sporadic diffuse leucoencephalopathy with axonal spheroids: report of a profuse and rapid cortical-spinal degeneration.}, author = {De Paula A.M. and Michel B.F. and Dickson D.W. and Wszolek Z.K. and Pellissier J-F.}, doi = {10.1007/s10072-011-0817-8}, year = {2011}, date = {2011-10-18}, journal = {Neurological Sciences}, volume = {33}, number = {4}, pages = {905-909}, abstract = {Diffuse leucoencephalopathy with axonal spheroids (DLS) is a rare disease affecting the white matter leading to dementia and progressive motor impairment. The neuropathological hallmark includes axonal swelling and spheroids as well as myelin loss. We report a case of a 46-year-old man with memory deficit and behavioral changes followed by a rapid cognitive decline and pyramidal syndrome. Head magnetic resonance imaging showed cortical atrophy of the brain and symmetric corticospinal tract involvement. He died 4 years after the first symptoms. Autopsy was performed and the brain revealed cortical and corpus callosum atrophy, a grayish granular appearance of the white matter and ventricular enlargement. Myelin stains showed a significant demyelination of the centrum ovale and corticospinal tract. Such degeneration was accompanied by axonal loss, axonal swelling, and numerous spheroids. There was no pigment overload or inflammation. We discuss this new DLS case with bilateral, severe, and rapid cortical-spinal involvement.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Diffuse leucoencephalopathy with axonal spheroids (DLS) is a rare disease affecting the white matter leading to dementia and progressive motor impairment. The neuropathological hallmark includes axonal swelling and spheroids as well as myelin loss. We report a case of a 46-year-old man with memory deficit and behavioral changes followed by a rapid cognitive decline and pyramidal syndrome. Head magnetic resonance imaging showed cortical atrophy of the brain and symmetric corticospinal tract involvement. He died 4 years after the first symptoms. Autopsy was performed and the brain revealed cortical and corpus callosum atrophy, a grayish granular appearance of the white matter and ventricular enlargement. Myelin stains showed a significant demyelination of the centrum ovale and corticospinal tract. Such degeneration was accompanied by axonal loss, axonal swelling, and numerous spheroids. There was no pigment overload or inflammation. We discuss this new DLS case with bilateral, severe, and rapid cortical-spinal involvement. |
Claude Touzet The Illusion of Internal Joy Book Chapter J. Schmidhuber K.R. Thórisson, ; Looks, M (Ed.): 6830 , p. 357-362, Springer Verlag, Lecture Notes in Artificial Intelligence, 2011, ISBN: 9783642228872. @inbook{b, title = {The Illusion of Internal Joy}, author = {Claude Touzet}, editor = {J. Schmidhuber, K.R. Thórisson, and M. Looks}, url = {http://www.touzet.org/Claude/Web-Fac-Claude/Publi/AGI-Google-2011-Touzet.pdf}, isbn = {9783642228872}, year = {2011}, date = {2011-08-31}, volume = {6830}, pages = {357-362}, publisher = {Springer Verlag}, edition = {Lecture Notes in Artificial Intelligence}, series = {LNAI}, abstract = {J. Schmidhuber proposes a "theory of fun & intrinsic motivation & creativity" that he has developed over the last two decades. This theory is precise enough to allow the programming of artificial agents exhibiting the requested behaviors. Schmidhuber's theory relies on an explicit 'internal joy drive' implemented by an 'information compression indicator'. In this paper, we show that this indicator is not necessary as soon as the 'brain' implementation involves associative memories, i.e., hierarchical cortical maps. The 'compression factor' is replaced by the 'smallest common activation pattern' in our framework, with the advantage of an immediate and plausible neural implementation. Our conclusion states that the 'internal joy' is an illusion. This remind us of the eliminative materialism position which claims that 'free-will' is also an illusion.}, keywords = {}, pubstate = {published}, tppubtype = {inbook} } J. Schmidhuber proposes a "theory of fun & intrinsic motivation & creativity" that he has developed over the last two decades. This theory is precise enough to allow the programming of artificial agents exhibiting the requested behaviors. Schmidhuber's theory relies on an explicit 'internal joy drive' implemented by an 'information compression indicator'. In this paper, we show that this indicator is not necessary as soon as the 'brain' implementation involves associative memories, i.e., hierarchical cortical maps. The 'compression factor' is replaced by the 'smallest common activation pattern' in our framework, with the advantage of an immediate and plausible neural implementation. Our conclusion states that the 'internal joy' is an illusion. This remind us of the eliminative materialism position which claims that 'free-will' is also an illusion. |
Abraham J.D.; Calvayrac-Pawlowski S.; Cobo S.; Salvetat N.; Vicat G.; Molina L.; Touchon J.; Michel B.F.; Molina F.; Verdier J-M.; Fareh J.; Mourton-Gilles C. Combined measurement of PEDF, haptoglobin and tau in cerebrospinal fluid improves the diagnostic discrimination between Alzheimer’s disease and other dementias. Article de journal Biomarkers, 16 (2), p. 161-171, 2011. @article{Abraham2011, title = { Combined measurement of PEDF, haptoglobin and tau in cerebrospinal fluid improves the diagnostic discrimination between Alzheimer’s disease and other dementias.}, author = {Abraham J.D. and Calvayrac-Pawlowski S. and Cobo S. and Salvetat N. and Vicat G. and Molina L. and Touchon J. and Michel B.F. and Molina F. and Verdier J-M. and Fareh J. and Mourton-Gilles C.}, doi = {10.3109/1354750X.2010.536995}, year = {2011}, date = {2011-02-17}, journal = {Biomarkers}, volume = {16}, number = {2}, pages = {161-171}, abstract = {Using proteomic approach in cerebrospinal fluid (CSF) we identified pigment epithelium-derived factor (PEDF) and Haptoglobin (Hp) as putative markers that could discriminate between AD and other dementias. ELISA assays were developed to measure the levels of PEDF and Hp in CSF from patients with AD (AD, n=27), non-AD (NAD, n=30) and in non-demented patients (ND, n=27). The combined assessment of PEDF, Hp and Tau levels, using Iterative Marginal Optimization, improved the differential diagnosis of AD, especially in patients with moderate to severe dementia (p<0.002). This pilot study highlights the probable different contribution of oxidative mechanisms in dementia.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Using proteomic approach in cerebrospinal fluid (CSF) we identified pigment epithelium-derived factor (PEDF) and Haptoglobin (Hp) as putative markers that could discriminate between AD and other dementias. ELISA assays were developed to measure the levels of PEDF and Hp in CSF from patients with AD (AD, n=27), non-AD (NAD, n=30) and in non-demented patients (ND, n=27). The combined assessment of PEDF, Hp and Tau levels, using Iterative Marginal Optimization, improved the differential diagnosis of AD, especially in patients with moderate to severe dementia (p<0.002). This pilot study highlights the probable different contribution of oxidative mechanisms in dementia. |
Marina Martinez; Jean-Michel Brezun; Christian Xerri Sensorimotor experience influences recovery of forelimb abilities but not tissue loss after focal cortical compression in adult rats Article de journal PloS one, 6 (2), p. e16726, 2011, ISSN: 1932-6203. @article{martinez_sensorimotor_2011, title = {Sensorimotor experience influences recovery of forelimb abilities but not tissue loss after focal cortical compression in adult rats}, author = { Marina Martinez and Jean-Michel Brezun and Christian Xerri}, issn = {1932-6203}, year = {2011}, date = {2011-01-01}, journal = {PloS one}, volume = {6}, number = {2}, pages = {e16726}, abstract = {Sensorimotor activity has been shown to play a key role in functional outcome after extensive brain damage. This study was aimed at assessing the influence of sensorimotor experience through subject-environment interactions on the time course of both lesion and gliosis volumes as well as on the recovery of forelimb sensorimotor abilities following focal cortical injury. The lesion consisted of a cortical compression targeting the forepaw representational area within the primary somatosensory cortex of adult rats. After the cortical lesion, rats were randomly subjected to various postlesion conditions: unilateral C5-C6 dorsal root transection depriving the contralateral cortex from forepaw somatosensory inputs, standard housing or an enriched environment promoting sensorimotor experience and social interactions. Behavioral tests were used to assess forelimb placement during locomotion, forelimb-use asymmetry, and forepaw tactile sensitivity. For each group, the time course of tissue loss was described and the gliosis volume over the first postoperative month was evaluated using an unbiased stereological method. Consistent with previous studies, recovery of behavioral abilities was found to depend on post-injury experience. Indeed, increased sensorimotor activity initiated early in an enriched environment induced a rapid and more complete behavioral recovery compared with standard housing. In contrast, severe deprivation of peripheral sensory inputs led to a delayed and only partial sensorimotor recovery. The dorsal rhizotomy was found to increase the perilesional gliosis in comparison to standard or enriched environments. These findings provide further evidence that early sensory experience has a beneficial influence on the onset and time course of functional recovery after focal brain injury.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Sensorimotor activity has been shown to play a key role in functional outcome after extensive brain damage. This study was aimed at assessing the influence of sensorimotor experience through subject-environment interactions on the time course of both lesion and gliosis volumes as well as on the recovery of forelimb sensorimotor abilities following focal cortical injury. The lesion consisted of a cortical compression targeting the forepaw representational area within the primary somatosensory cortex of adult rats. After the cortical lesion, rats were randomly subjected to various postlesion conditions: unilateral C5-C6 dorsal root transection depriving the contralateral cortex from forepaw somatosensory inputs, standard housing or an enriched environment promoting sensorimotor experience and social interactions. Behavioral tests were used to assess forelimb placement during locomotion, forelimb-use asymmetry, and forepaw tactile sensitivity. For each group, the time course of tissue loss was described and the gliosis volume over the first postoperative month was evaluated using an unbiased stereological method. Consistent with previous studies, recovery of behavioral abilities was found to depend on post-injury experience. Indeed, increased sensorimotor activity initiated early in an enriched environment induced a rapid and more complete behavioral recovery compared with standard housing. In contrast, severe deprivation of peripheral sensory inputs led to a delayed and only partial sensorimotor recovery. The dorsal rhizotomy was found to increase the perilesional gliosis in comparison to standard or enriched environments. These findings provide further evidence that early sensory experience has a beneficial influence on the onset and time course of functional recovery after focal brain injury. |
Véronique Paban; Caroline Chambon; Fernand Farioli; Béatrice Alescio-Lautier Gene regulation in the rat prefrontal cortex after learning with or without cholinergic insult Article de journal Neurobiology of Learning and Memory, 95 (4), p. 441–452, 2011, ISSN: 1095-9564. @article{paban_gene_2011, title = {Gene regulation in the rat prefrontal cortex after learning with or without cholinergic insult}, author = { Véronique Paban and Caroline Chambon and Fernand Farioli and Béatrice Alescio-Lautier}, issn = {1095-9564}, year = {2011}, date = {2011-01-01}, journal = {Neurobiology of Learning and Memory}, volume = {95}, number = {4}, pages = {441--452}, abstract = {The prefrontal cortex is essential for a wide variety of higher functions, including attention and memory. Cholinergic neurons are thought to be of prime importance in the modulation of these processes. Degeneration of forebrain cholinergic neurons has been linked to several neurological disorders. The present study was designed to identify genes and networks in rat prefrontal cortex that are associated with learning and cholinergic-loss-memory deficit. Affymetrix microarray technology was used to screen gene expression changes in rats submitted or not to 192 IgG-saporin immunolesion of cholinergic basal forebrain and trained in spatial/object novelty tasks. Results showed learning processes were associated with significant expression of genes, which were organized in several clusters of highly correlated genes and would be involved in biological processes such as intracellular signaling process, transcription regulation, and filament organization and axon guidance. Memory loss following cortical cholinergic deafferentation was associated with significant expression of genes belonging to only one clearly delineated cluster and would be involved in biological processes related to cytoskeleton organization and proliferation, and glial and vascular remodeling, i.e., in processes associated with brain repair after injury.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The prefrontal cortex is essential for a wide variety of higher functions, including attention and memory. Cholinergic neurons are thought to be of prime importance in the modulation of these processes. Degeneration of forebrain cholinergic neurons has been linked to several neurological disorders. The present study was designed to identify genes and networks in rat prefrontal cortex that are associated with learning and cholinergic-loss-memory deficit. Affymetrix microarray technology was used to screen gene expression changes in rats submitted or not to 192 IgG-saporin immunolesion of cholinergic basal forebrain and trained in spatial/object novelty tasks. Results showed learning processes were associated with significant expression of genes, which were organized in several clusters of highly correlated genes and would be involved in biological processes such as intracellular signaling process, transcription regulation, and filament organization and axon guidance. Memory loss following cortical cholinergic deafferentation was associated with significant expression of genes belonging to only one clearly delineated cluster and would be involved in biological processes related to cytoskeleton organization and proliferation, and glial and vascular remodeling, i.e., in processes associated with brain repair after injury. |
Caroline Blanchard; Régine Roll; Jean-Pierre Roll; Anne Kavounoudias Combined contribution of tactile and proprioceptive feedback to hand movement perception Article de journal Brain Research, 1382 , p. 219–229, 2011, ISSN: 1872-6240. @article{blanchard_combined_2011, title = {Combined contribution of tactile and proprioceptive feedback to hand movement perception}, author = { Caroline Blanchard and Régine Roll and Jean-Pierre Roll and Anne Kavounoudias}, issn = {1872-6240}, year = {2011}, date = {2011-01-01}, journal = {Brain Research}, volume = {1382}, pages = {219--229}, abstract = {Here we investigated how the tactile modality is used along with muscle proprioception in hand movement perception, whether these two sensory inputs are centrally integrated and whether they work complementarily or concurrently. The illusory right hand rotations induced in eleven volunteers by a textured disk scrolling under their hand in two directions at three velocities and/or by mechanical vibration applied to their wrist muscles at three frequencies were compared. The kinesthetic illusions were copied by the subjects on-line with their left hand. Results: 1) in all the subjects, tactile stimulation alone induced an illusory hand rotation in the opposite direction to that of the disk, and the velocity of the illusion increased non-linearly with the disk velocity: the highest gain (the illusion velocity to disk velocity ratio) occurred at the slowest disk rotation; 2) adding a consistent proprioceptive stimulus increased the perceptual effects, whereas adding a conflicting proprioceptive stimulus of increasing frequency gradually decreased the tactile illusions and reversed their initial direction; 3) under both consistent and conflicting conditions, only strong proprioceptive stimulation significantly affected the gain of the resulting illusions, whereas the largest gain always occurred at low tactile stimulation levels when the illusory movements were in the same direction as the tactile-induced illusion. Tactile information may equal or even override muscle proprioceptive information in the perception of relatively small, slow hand movements. These two somatosensory inputs may be integrated complementarily, depending on their respective relevance to the task of accurately perceiving one's own hand movements.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Here we investigated how the tactile modality is used along with muscle proprioception in hand movement perception, whether these two sensory inputs are centrally integrated and whether they work complementarily or concurrently. The illusory right hand rotations induced in eleven volunteers by a textured disk scrolling under their hand in two directions at three velocities and/or by mechanical vibration applied to their wrist muscles at three frequencies were compared. The kinesthetic illusions were copied by the subjects on-line with their left hand. Results: 1) in all the subjects, tactile stimulation alone induced an illusory hand rotation in the opposite direction to that of the disk, and the velocity of the illusion increased non-linearly with the disk velocity: the highest gain (the illusion velocity to disk velocity ratio) occurred at the slowest disk rotation; 2) adding a consistent proprioceptive stimulus increased the perceptual effects, whereas adding a conflicting proprioceptive stimulus of increasing frequency gradually decreased the tactile illusions and reversed their initial direction; 3) under both consistent and conflicting conditions, only strong proprioceptive stimulation significantly affected the gain of the resulting illusions, whereas the largest gain always occurred at low tactile stimulation levels when the illusory movements were in the same direction as the tactile-induced illusion. Tactile information may equal or even override muscle proprioceptive information in the perception of relatively small, slow hand movements. These two somatosensory inputs may be integrated complementarily, depending on their respective relevance to the task of accurately perceiving one's own hand movements. |
Ibtihel Smeti; Etienne Savary; Vincent Capelle; Jean Philippe Hugnot; Alain Uziel; Azel Zine Expression of candidate markers for stem/progenitor cells in the inner ears of developing and adult GFAP and nestin promoter-GFP transgenic mice Article de journal Gene expression patterns: GEP, 11 (1-2), p. 22–32, 2011, ISSN: 1872-7298. @article{smeti_expression_2011, title = {Expression of candidate markers for stem/progenitor cells in the inner ears of developing and adult GFAP and nestin promoter-GFP transgenic mice}, author = { Ibtihel Smeti and Etienne Savary and Vincent Capelle and Jean Philippe Hugnot and Alain Uziel and Azel Zine}, issn = {1872-7298}, year = {2011}, date = {2011-01-01}, journal = {Gene expression patterns: GEP}, volume = {11}, number = {1-2}, pages = {22--32}, abstract = {Loss of hair cells in the mammalian cochlea leads to permanent sensori-neural hearing loss. Hair cells degenerate and their places are taken by phalangeal scars formed by non-sensory supporting cells. Current data indicate that early postnatal post-mitotic supporting cells can proliferate and differentiate into hair cell-like cells in culture. In this study, we used GFAP and nestin promoter-GFP transgenic mice in combination with other stem cell markers to characterize supporting cell subtypes in the postnatal day-3 (P3) and adult organs of Corti with potential stem/progenitor cell phenotype. In P3 organ of Corti, we show GFAP-GFP signal in all the supporting cell subtypes while the nestin-GFP was restricted to the supporting cells in the inner hair cell area. At this stage, GFAP and selected stem/progenitor markers displayed overlapping expression pattern in the supporting cell population. In the adult, GFAP expression is down-regulated from the supporting cells in the outer hair cell area and nestin expression is down-regulated in the supporting cells of the inner hair cell area. Sox2 and Jagged1 expression is maintained in the mature supporting cells, while Abcg2 was down-regulated in these cells. In contrast, GFAP and Abcg2 expression was up-regulated in the inner sulcus limbal cells outside the mature organ of Corti's area. Using quantitative reverse transcription-PCR, we found a decrease in transcripts for Jagged1 and Sox2 in adult cochleae. Our findings suggest that the loss of regenerative capacity of the adult organ of Corti is related to down-regulation of stem/progenitor key-markers from the mature supporting cells.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Loss of hair cells in the mammalian cochlea leads to permanent sensori-neural hearing loss. Hair cells degenerate and their places are taken by phalangeal scars formed by non-sensory supporting cells. Current data indicate that early postnatal post-mitotic supporting cells can proliferate and differentiate into hair cell-like cells in culture. In this study, we used GFAP and nestin promoter-GFP transgenic mice in combination with other stem cell markers to characterize supporting cell subtypes in the postnatal day-3 (P3) and adult organs of Corti with potential stem/progenitor cell phenotype. In P3 organ of Corti, we show GFAP-GFP signal in all the supporting cell subtypes while the nestin-GFP was restricted to the supporting cells in the inner hair cell area. At this stage, GFAP and selected stem/progenitor markers displayed overlapping expression pattern in the supporting cell population. In the adult, GFAP expression is down-regulated from the supporting cells in the outer hair cell area and nestin expression is down-regulated in the supporting cells of the inner hair cell area. Sox2 and Jagged1 expression is maintained in the mature supporting cells, while Abcg2 was down-regulated in these cells. In contrast, GFAP and Abcg2 expression was up-regulated in the inner sulcus limbal cells outside the mature organ of Corti's area. Using quantitative reverse transcription-PCR, we found a decrease in transcripts for Jagged1 and Sox2 in adult cochleae. Our findings suggest that the loss of regenerative capacity of the adult organ of Corti is related to down-regulation of stem/progenitor key-markers from the mature supporting cells. |
L. Heydrich; Christophe Lopez; M. Seeck; O. Blanke Partial and full own-body illusions of epileptic origin in a child with right temporoparietal epilepsy Article de journal Epilepsy Behav, 20 , p. 583–6, 2011, ISSN: 1525-5069 (Electronic) 1525-5050 (Linking), (3). @article{heydrich_partial_2011, title = {Partial and full own-body illusions of epileptic origin in a child with right temporoparietal epilepsy}, author = { L. Heydrich and Christophe Lopez and M. Seeck and O. Blanke}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21334265}, issn = {1525-5069 (Electronic) 1525-5050 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Epilepsy Behav}, volume = {20}, pages = {583--6}, abstract = {Partial and full own-body illusions of neurological origin have been claimed crucial to understand the contribution of bodily experience and perception to self-consciousness. Whereas partial body illusions are relatively common and well defined, much less is known about full own-body illusions, and even less is known about these illusions in children. Here we describe a 10-year-old patient with the association of partial and full own-body illusions (somatoparaphrenia and out-of-body experience) that occurred sequentially during an epileptic seizure caused by right temporoparietal epilepsy. This report shows that partial and full own-body illusions share functional and neuroanatomical properties and highlights the importance of the right temporoparietal junction for bodily self-consciousness. This is the first report of out-of-body experiences in a child with focal epilepsy.}, note = {3}, keywords = {}, pubstate = {published}, tppubtype = {article} } Partial and full own-body illusions of neurological origin have been claimed crucial to understand the contribution of bodily experience and perception to self-consciousness. Whereas partial body illusions are relatively common and well defined, much less is known about full own-body illusions, and even less is known about these illusions in children. Here we describe a 10-year-old patient with the association of partial and full own-body illusions (somatoparaphrenia and out-of-body experience) that occurred sequentially during an epileptic seizure caused by right temporoparietal epilepsy. This report shows that partial and full own-body illusions share functional and neuroanatomical properties and highlights the importance of the right temporoparietal junction for bodily self-consciousness. This is the first report of out-of-body experiences in a child with focal epilepsy. |
Christophe Lopez; M. R. Mercier; P. Halje; O. Blanke Spatiotemporal dynamics of visual vertical judgments: early and late brain mechanisms as revealed by high-density electrical neuroimaging Article de journal Neuroscience, 181 , p. 134–49, 2011, ISSN: 1873-7544 (Electronic) 0306-4522 (Linking). @article{lopez_spatiotemporal_2011, title = {Spatiotemporal dynamics of visual vertical judgments: early and late brain mechanisms as revealed by high-density electrical neuroimaging}, author = { Christophe Lopez and M. R. Mercier and P. Halje and O. Blanke}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21315805}, issn = {1873-7544 (Electronic) 0306-4522 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Neuroscience}, volume = {181}, pages = {134--49}, abstract = {Constructing and updating an internal model of verticality is fundamental for maintaining an erect posture and facilitating visuo-spatial processing. The judgment of the visual vertical (VV) has been intensively studied in psychophysical investigations and relies mainly on the integration of visual and vestibular signals, although a contribution of postural and somatosensory signals has been reported. Here we used high-density 192-channel evoked potential (EP) mapping and distributed source localization techniques to reveal the neural mechanisms of VV judgments. VV judgments (judging the orientation of visual lines with respect to the subjective vertical) were performed with and without a tilted visual frame. EP mapping revealed a sequence of neural processing steps (EP maps) of which two were specific for VV judgments. An early EP map, observed at approximately 75-105 ms post-stimulus, was localized in right lateral temporo-occipital cortex. A later EP map ( approximately 260-290 ms) was localized in bilateral temporo-occipital and parieto-occipital cortex. These data suggest that early VV-related neural processing involves the lateral and ventral visual stream and is related to visual processing concerning orientation, attention and comparison. The later, more dorsal, activation involves multimodal cortex subtending a constantly available and updated internal model of the vertical that we can refer to for the control of one's posture, actions, and visuo-spatial processing.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Constructing and updating an internal model of verticality is fundamental for maintaining an erect posture and facilitating visuo-spatial processing. The judgment of the visual vertical (VV) has been intensively studied in psychophysical investigations and relies mainly on the integration of visual and vestibular signals, although a contribution of postural and somatosensory signals has been reported. Here we used high-density 192-channel evoked potential (EP) mapping and distributed source localization techniques to reveal the neural mechanisms of VV judgments. VV judgments (judging the orientation of visual lines with respect to the subjective vertical) were performed with and without a tilted visual frame. EP mapping revealed a sequence of neural processing steps (EP maps) of which two were specific for VV judgments. An early EP map, observed at approximately 75-105 ms post-stimulus, was localized in right lateral temporo-occipital cortex. A later EP map ( approximately 260-290 ms) was localized in bilateral temporo-occipital and parieto-occipital cortex. These data suggest that early VV-related neural processing involves the lateral and ventral visual stream and is related to visual processing concerning orientation, attention and comparison. The later, more dorsal, activation involves multimodal cortex subtending a constantly available and updated internal model of the vertical that we can refer to for the control of one's posture, actions, and visuo-spatial processing. |
Christophe Lopez; D. Vibert; F. W. Mast Can imagined whole-body rotations improve vestibular compensation? Article de journal Med Hypotheses, 76 , p. 816–9, 2011, ISSN: 1532-2777 (Electronic) 0306-9877 (Linking), (6). @article{lopez_can_2011, title = {Can imagined whole-body rotations improve vestibular compensation?}, author = { Christophe Lopez and D. Vibert and F. W. Mast}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21398044}, issn = {1532-2777 (Electronic) 0306-9877 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Med Hypotheses}, volume = {76}, pages = {816--9}, abstract = {Unilateral damage to the labyrinth and the vestibular nerve cause rotational vertigo, postural imbalance, oculomotor disorders and spatial disorientation. Electrophysiological investigations in animals revealed that such deficits are partly due to imbalanced spontaneous activity and sensitivity to motion in neurons located in the ipsilesional and contralesional vestibular nuclei. Neurophysiological reorganizations taking place in the vestibular nuclei are the basis of the decline of the symptoms over time, a phenomenon known as vestibular compensation. Vestibular compensation is facilitated by motor activity and sensory experience, and current rehabilitation programs favor physical activity during the acute stage of a unilateral vestibular loss. Unfortunately, vestibular-defective patients tend to develop strategies in order to avoid movements causing imbalance and nausea (in particular body movements towards the lesioned side), which impedes vestibular compensation. Neuroanatomical evidence suggests a cortical control of postural and oculomotor reflexes based on corticofugal projections to the vestibular nuclei and, therefore, the possibility to manipulate vestibular functions through top-down mechanisms. Based on evidence from neuroimaging studies showing that imagined whole-body movements can activate part of the vestibular cortex, we propose that mental imagery of whole-body rotations to the lesioned and to the healthy side will help rebalancing the activity in the ipsilesional and contralesional vestibular nuclei. Whether imagined whole-body rotations can improve vestibular compensation could be tested in a randomized controlled study in such patients beneficiating, or not, from a mental imagery training. If validated, this hypothesis will help developing a method contributing to reduce postural instability and falls in vestibular-defective patients. Imagined whole-body rotations thus could provide a simple, safe, home-based and self-administered therapeutic method with the potential to overcome the inconvenience related to physical movements.}, note = {6}, keywords = {}, pubstate = {published}, tppubtype = {article} } Unilateral damage to the labyrinth and the vestibular nerve cause rotational vertigo, postural imbalance, oculomotor disorders and spatial disorientation. Electrophysiological investigations in animals revealed that such deficits are partly due to imbalanced spontaneous activity and sensitivity to motion in neurons located in the ipsilesional and contralesional vestibular nuclei. Neurophysiological reorganizations taking place in the vestibular nuclei are the basis of the decline of the symptoms over time, a phenomenon known as vestibular compensation. Vestibular compensation is facilitated by motor activity and sensory experience, and current rehabilitation programs favor physical activity during the acute stage of a unilateral vestibular loss. Unfortunately, vestibular-defective patients tend to develop strategies in order to avoid movements causing imbalance and nausea (in particular body movements towards the lesioned side), which impedes vestibular compensation. Neuroanatomical evidence suggests a cortical control of postural and oculomotor reflexes based on corticofugal projections to the vestibular nuclei and, therefore, the possibility to manipulate vestibular functions through top-down mechanisms. Based on evidence from neuroimaging studies showing that imagined whole-body movements can activate part of the vestibular cortex, we propose that mental imagery of whole-body rotations to the lesioned and to the healthy side will help rebalancing the activity in the ipsilesional and contralesional vestibular nuclei. Whether imagined whole-body rotations can improve vestibular compensation could be tested in a randomized controlled study in such patients beneficiating, or not, from a mental imagery training. If validated, this hypothesis will help developing a method contributing to reduce postural instability and falls in vestibular-defective patients. Imagined whole-body rotations thus could provide a simple, safe, home-based and self-administered therapeutic method with the potential to overcome the inconvenience related to physical movements. |
Christophe Lopez; O. Blanke The thalamocortical vestibular system in animals and humans Article de journal Brain Res Rev, 67 , p. 119–146, 2011, ISSN: 1872-6321 (Electronic) 0165-0173 (Linking), (119). @article{lopez_thalamocortical_2011, title = {The thalamocortical vestibular system in animals and humans}, author = { Christophe Lopez and O. Blanke}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21223979}, issn = {1872-6321 (Electronic) 0165-0173 (Linking)}, year = {2011}, date = {2011-01-01}, journal = {Brain Res Rev}, volume = {67}, pages = {119--146}, abstract = {The vestibular system provides the brain with sensory signals about three-dimensional head rotations and translations. These signals are important for postural and oculomotor control, as well as for spatial and bodily perception and cognition, and they are subtended by pathways running from the vestibular nuclei to the thalamus, cerebellum and the "vestibular cortex." The present review summarizes current knowledge on the anatomy of the thalamocortical vestibular system and discusses data from electrophysiology and neuroanatomy in animals by comparing them with data from neuroimagery and neurology in humans. Multiple thalamic nuclei are involved in vestibular processing, including the ventroposterior complex, the ventroanterior-ventrolateral complex, the intralaminar nuclei and the posterior nuclear group (medial and lateral geniculate nuclei, pulvinar). These nuclei contain multisensory neurons that process and relay vestibular, proprioceptive and visual signals to the vestibular cortex. In non-human primates, the parieto-insular vestibular cortex (PIVC) has been proposed as the core vestibular region. Yet, vestibular responses have also been recorded in the somatosensory cortex (area 2v, 3av), intraparietal sulcus, posterior parietal cortex (area 7), area MST, frontal cortex, cingulum and hippocampus. We analyze the location of the corresponding regions in humans, and especially the human PIVC, by reviewing neuroimaging and clinical work. The widespread vestibular projections to the multimodal human PIVC, somatosensory cortex, area MST, intraparietal sulcus and hippocampus explain the large influence of vestibular signals on self-motion perception, spatial navigation, internal models of gravity, one's body perception and bodily self-consciousness.}, note = {119}, keywords = {}, pubstate = {published}, tppubtype = {article} } The vestibular system provides the brain with sensory signals about three-dimensional head rotations and translations. These signals are important for postural and oculomotor control, as well as for spatial and bodily perception and cognition, and they are subtended by pathways running from the vestibular nuclei to the thalamus, cerebellum and the "vestibular cortex." The present review summarizes current knowledge on the anatomy of the thalamocortical vestibular system and discusses data from electrophysiology and neuroanatomy in animals by comparing them with data from neuroimagery and neurology in humans. Multiple thalamic nuclei are involved in vestibular processing, including the ventroposterior complex, the ventroanterior-ventrolateral complex, the intralaminar nuclei and the posterior nuclear group (medial and lateral geniculate nuclei, pulvinar). These nuclei contain multisensory neurons that process and relay vestibular, proprioceptive and visual signals to the vestibular cortex. In non-human primates, the parieto-insular vestibular cortex (PIVC) has been proposed as the core vestibular region. Yet, vestibular responses have also been recorded in the somatosensory cortex (area 2v, 3av), intraparietal sulcus, posterior parietal cortex (area 7), area MST, frontal cortex, cingulum and hippocampus. We analyze the location of the corresponding regions in humans, and especially the human PIVC, by reviewing neuroimaging and clinical work. The widespread vestibular projections to the multimodal human PIVC, somatosensory cortex, area MST, intraparietal sulcus and hippocampus explain the large influence of vestibular signals on self-motion perception, spatial navigation, internal models of gravity, one's body perception and bodily self-consciousness. |
Clément Menuet; Yves Cazals; Christian Gestreau; Peter Borghgraef; Lies Gielis; Mathias Dutschmann; Fred Van Leuven; Gérard Hilaire Age-related impairment of ultrasonic vocalization in TauṖ301L mice: possible implication for progressive language disorders Article de journal PloS one, 6 (10), p. e25770, 2011, ISSN: 1932-6203. @article{menuet_age-related_2011, title = {Age-related impairment of ultrasonic vocalization in TauṖ301L mice: possible implication for progressive language disorders}, author = { Clément Menuet and Yves Cazals and Christian Gestreau and Peter Borghgraef and Lies Gielis and Mathias Dutschmann and Fred Van Leuven and Gérard Hilaire}, issn = {1932-6203}, year = {2011}, date = {2011-01-01}, journal = {PloS one}, volume = {6}, number = {10}, pages = {e25770}, abstract = {BACKGROUND: Tauopathies, including Alzheimer's Disease, are the most frequent neurodegenerative diseases in elderly people and cause various cognitive, behavioural and motor defects, but also progressive language disorders. For communication and social interactions, mice produce ultrasonic vocalization (USV) via expiratory airflow through the larynx. We examined USV of Tau.P301L mice, a mouse model for tauopathy expressing human mutant tau protein and developing cognitive, motor and upper airway defects. METHODOLOGY/PRINCIPAL FINDINGS: At age 4-5 months, Tau.P301L mice had normal USV, normal expiratory airflow and no brainstem tauopathy. At age 8-10 months, Tau.P301L mice presented impaired USV, reduced expiratory airflow and severe tauopathy in the periaqueductal gray, Kolliker-Fuse and retroambiguus nuclei. Tauopathy in these nuclei that control upper airway function and vocalization correlates well with the USV impairment of old Tau.P301L mice. CONCLUSIONS: In a mouse model for tauopathy, we report for the first time an age-related impairment of USV that correlates with tauopathy in midbrain and brainstem areas controlling vocalization. The vocalization disorder of old Tau.P301L mice could be, at least in part, reminiscent of language disorders of elderly suffering tauopathy.}, keywords = {}, pubstate = {published}, tppubtype = {article} } BACKGROUND: Tauopathies, including Alzheimer's Disease, are the most frequent neurodegenerative diseases in elderly people and cause various cognitive, behavioural and motor defects, but also progressive language disorders. For communication and social interactions, mice produce ultrasonic vocalization (USV) via expiratory airflow through the larynx. We examined USV of Tau.P301L mice, a mouse model for tauopathy expressing human mutant tau protein and developing cognitive, motor and upper airway defects. METHODOLOGY/PRINCIPAL FINDINGS: At age 4-5 months, Tau.P301L mice had normal USV, normal expiratory airflow and no brainstem tauopathy. At age 8-10 months, Tau.P301L mice presented impaired USV, reduced expiratory airflow and severe tauopathy in the periaqueductal gray, Kolliker-Fuse and retroambiguus nuclei. Tauopathy in these nuclei that control upper airway function and vocalization correlates well with the USV impairment of old Tau.P301L mice. CONCLUSIONS: In a mouse model for tauopathy, we report for the first time an age-related impairment of USV that correlates with tauopathy in midbrain and brainstem areas controlling vocalization. The vocalization disorder of old Tau.P301L mice could be, at least in part, reminiscent of language disorders of elderly suffering tauopathy. |
Sophie Dutheil; Michel Lacour; Brahim Tighilet [Discovering a new functional neurogenic zone: the vestibular nuclei of the brainstem] Article de journal Médecine sciences: M/S, 27 (6-7), p. 605–613, 2011, ISSN: 0767-0974. @article{dutheil_[discovering_2011, title = {[Discovering a new functional neurogenic zone: the vestibular nuclei of the brainstem]}, author = { Sophie Dutheil and Michel Lacour and Brahim Tighilet}, issn = {0767-0974}, year = {2011}, date = {2011-01-01}, journal = {Médecine sciences: M/S}, volume = {27}, number = {6-7}, pages = {605--613}, abstract = {The adult mammal brain is mostly considered as non-neurogenic, except in the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus, where ongoing neurogenesis occurs. However, anti-neurogenic influences can be removed in pathological conditions or after specific injury. That is what happens in a model of unilateral vestibular neurectomy (UVN) that mimics human pathology in adult cats. We showed for the first time that a UVN promoted an intense reactive cell proliferation in the deafferented vestibular nuclei located in the brainstem. The new cells survived up to one month, differentiated into glial cells - microglia or astrocytes - or GABAergic neurons, so highlighting a GABAergic neurogenesis. Surprisingly, we further showed that post-UVN reactive cell proliferation contributed successfully to fine restoration of vestibular posturo-locomotor functions. In conclusion, these pioneering studies bring new pieces of a promising puzzle in both stem cell and vestibular therapy domains.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The adult mammal brain is mostly considered as non-neurogenic, except in the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus, where ongoing neurogenesis occurs. However, anti-neurogenic influences can be removed in pathological conditions or after specific injury. That is what happens in a model of unilateral vestibular neurectomy (UVN) that mimics human pathology in adult cats. We showed for the first time that a UVN promoted an intense reactive cell proliferation in the deafferented vestibular nuclei located in the brainstem. The new cells survived up to one month, differentiated into glial cells - microglia or astrocytes - or GABAergic neurons, so highlighting a GABAergic neurogenesis. Surprisingly, we further showed that post-UVN reactive cell proliferation contributed successfully to fine restoration of vestibular posturo-locomotor functions. In conclusion, these pioneering studies bring new pieces of a promising puzzle in both stem cell and vestibular therapy domains. |
Sophie Dutheil; Michel Lacour; Brahim Tighilet Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage Article de journal PloS one, 6 (8), p. e22262, 2011, ISSN: 1932-6203. @article{dutheil_neurogenic_2011, title = {Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage}, author = { Sophie Dutheil and Michel Lacour and Brahim Tighilet}, issn = {1932-6203}, year = {2011}, date = {2011-01-01}, journal = {PloS one}, volume = {6}, number = {8}, pages = {e22262}, abstract = {Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology. |
Patrick Péruch; Christophe Lopez; Christine Redon-Zouiteni; Guy Escoffier; Alain Zeitoun; Mélanie Sanjuan; Arnaud Devèze; Jacques Magnan; Liliane Borel Vestibular information is necessary for maintaining metric properties of representational space: evidence from mental imagery Article de journal Neuropsychologia, 49 (11), p. 3136–3144, 2011, ISSN: 1873-3514. @article{peruch_vestibular_2011, title = {Vestibular information is necessary for maintaining metric properties of representational space: evidence from mental imagery}, author = { Patrick Péruch and Christophe Lopez and Christine Redon-Zouiteni and Guy Escoffier and Alain Zeitoun and Mélanie Sanjuan and Arnaud Devèze and Jacques Magnan and Liliane Borel}, issn = {1873-3514}, year = {2011}, date = {2011-01-01}, journal = {Neuropsychologia}, volume = {49}, number = {11}, pages = {3136--3144}, abstract = {The vestibular system contributes to a wide range of functions, from postural and oculomotor reflexes to spatial representation and cognition. Vestibular signals are important to maintain an internal, updated representation of the body position and movement in space. However, it is not clear to what extent they are also necessary to mentally simulate movement in situations that do not involve displacements of the body, as in mental imagery. The present study assessed how vestibular loss can affect object-based mental transformations (OMTs), i.e., imagined rotations or translations of objects relative to the environment. Participants performed one task of mental rotation of 3D-objects and two mental scanning tasks dealing with the ability to build and manipulate mental images that have metric properties. Menière's disease patients were tested before unilateral vestibular neurotomy and during the recovery period (1 week and 1 month). They were compared to healthy participants tested at similar time intervals and to bilateral vestibular-defective patients tested after the recovery period. Vestibular loss impaired all mental imagery tasks. Performance varied according to the extent of vestibular loss (bilateral patients were frequently the most impaired) and according to the time elapsed after unilateral vestibular neurotomy (deficits were stronger at the early stage after neurotomy and then gradually compensated). These findings indicate that vestibular signals are necessary to perform OMTs and provide the first demonstration of the critical role of vestibular signals in processing metric properties of mental representations. They suggest that vestibular loss disorganizes brain structures commonly involved in mental imagery, and more generally in mental representation.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The vestibular system contributes to a wide range of functions, from postural and oculomotor reflexes to spatial representation and cognition. Vestibular signals are important to maintain an internal, updated representation of the body position and movement in space. However, it is not clear to what extent they are also necessary to mentally simulate movement in situations that do not involve displacements of the body, as in mental imagery. The present study assessed how vestibular loss can affect object-based mental transformations (OMTs), i.e., imagined rotations or translations of objects relative to the environment. Participants performed one task of mental rotation of 3D-objects and two mental scanning tasks dealing with the ability to build and manipulate mental images that have metric properties. Menière's disease patients were tested before unilateral vestibular neurotomy and during the recovery period (1 week and 1 month). They were compared to healthy participants tested at similar time intervals and to bilateral vestibular-defective patients tested after the recovery period. Vestibular loss impaired all mental imagery tasks. Performance varied according to the extent of vestibular loss (bilateral patients were frequently the most impaired) and according to the time elapsed after unilateral vestibular neurotomy (deficits were stronger at the early stage after neurotomy and then gradually compensated). These findings indicate that vestibular signals are necessary to perform OMTs and provide the first demonstration of the critical role of vestibular signals in processing metric properties of mental representations. They suggest that vestibular loss disorganizes brain structures commonly involved in mental imagery, and more generally in mental representation. |
Christine Redon; Christophe Lopez; Laurence Bernard-Demanze; Michel Dumitrescu; Jacques Magnan; Michel Lacour; Liliane Borel Betahistine treatment improves the recovery of static symptoms in patients with unilateral vestibular loss Article de journal Journal of clinical pharmacology, 51 (4), p. 538–548, 2011, ISSN: 1552-4604. @article{redon_betahistine_2011, title = {Betahistine treatment improves the recovery of static symptoms in patients with unilateral vestibular loss}, author = { Christine Redon and Christophe Lopez and Laurence Bernard-Demanze and Michel Dumitrescu and Jacques Magnan and Michel Lacour and Liliane Borel}, issn = {1552-4604}, year = {2011}, date = {2011-01-01}, journal = {Journal of clinical pharmacology}, volume = {51}, number = {4}, pages = {538--548}, abstract = {Vestibular loss induces a combination of postural, oculomotor, and perceptive symptoms that are compensated over time. The aim of this study was to analyze the influence of betahistine dihydrochloride on vestibular compensation. A randomized, double-blind, placebo-controlled study was performed in Menière's disease patients who underwent a curative unilateral vestibular neurotomy (UVN). The effects of betahistine treatment were investigated on a broad spectrum of vestibular-induced changes resulting from vestibular loss: body sway, head orientation, ocular cyclotorsion, spontaneous nystagmus, verticality perception, and self-evaluation of the postural stability. The time course of the recovery was compared in 16 patients who received either a placebo or betahistine (24 mg b.i.d.) from 3 days up to 3 months after UVN. Patients were examined before (day -1) and after UVN (days 7, 30, and 90). Results indicate that betahistine reduces the time to recovery by 1 month or more depending on the tested functions. Betahistine was effective as soon as 4 days after treatment administration, and the effect remained during the whole compensation period (up to 3 months). The observed clinical effects may be attributed to an action of betahistine in rebalancing the neuronal activity between contralateral vestibular nuclei.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Vestibular loss induces a combination of postural, oculomotor, and perceptive symptoms that are compensated over time. The aim of this study was to analyze the influence of betahistine dihydrochloride on vestibular compensation. A randomized, double-blind, placebo-controlled study was performed in Menière's disease patients who underwent a curative unilateral vestibular neurotomy (UVN). The effects of betahistine treatment were investigated on a broad spectrum of vestibular-induced changes resulting from vestibular loss: body sway, head orientation, ocular cyclotorsion, spontaneous nystagmus, verticality perception, and self-evaluation of the postural stability. The time course of the recovery was compared in 16 patients who received either a placebo or betahistine (24 mg b.i.d.) from 3 days up to 3 months after UVN. Patients were examined before (day -1) and after UVN (days 7, 30, and 90). Results indicate that betahistine reduces the time to recovery by 1 month or more depending on the tested functions. Betahistine was effective as soon as 4 days after treatment administration, and the effect remained during the whole compensation period (up to 3 months). The observed clinical effects may be attributed to an action of betahistine in rebalancing the neuronal activity between contralateral vestibular nuclei. |
Publications 2011
Soleil Digital
2018-01-24T14:17:05+00:00
2011 |
Long-term progression of Alzheimer’s disease in patients under antidementia drugs. Article de journal Alzheimer's & Dementia, 7 (6), p. 579–592, 2011. |
Sporadic diffuse leucoencephalopathy with axonal spheroids: report of a profuse and rapid cortical-spinal degeneration. Article de journal Neurological Sciences, 33 (4), p. 905-909, 2011. |
The Illusion of Internal Joy Book Chapter J. Schmidhuber K.R. Thórisson, ; Looks, M (Ed.): 6830 , p. 357-362, Springer Verlag, Lecture Notes in Artificial Intelligence, 2011, ISBN: 9783642228872. |
Combined measurement of PEDF, haptoglobin and tau in cerebrospinal fluid improves the diagnostic discrimination between Alzheimer’s disease and other dementias. Article de journal Biomarkers, 16 (2), p. 161-171, 2011. |
Sensorimotor experience influences recovery of forelimb abilities but not tissue loss after focal cortical compression in adult rats Article de journal PloS one, 6 (2), p. e16726, 2011, ISSN: 1932-6203. |
Gene regulation in the rat prefrontal cortex after learning with or without cholinergic insult Article de journal Neurobiology of Learning and Memory, 95 (4), p. 441–452, 2011, ISSN: 1095-9564. |
Combined contribution of tactile and proprioceptive feedback to hand movement perception Article de journal Brain Research, 1382 , p. 219–229, 2011, ISSN: 1872-6240. |
Expression of candidate markers for stem/progenitor cells in the inner ears of developing and adult GFAP and nestin promoter-GFP transgenic mice Article de journal Gene expression patterns: GEP, 11 (1-2), p. 22–32, 2011, ISSN: 1872-7298. |
Partial and full own-body illusions of epileptic origin in a child with right temporoparietal epilepsy Article de journal Epilepsy Behav, 20 , p. 583–6, 2011, ISSN: 1525-5069 (Electronic) 1525-5050 (Linking), (3). |
Spatiotemporal dynamics of visual vertical judgments: early and late brain mechanisms as revealed by high-density electrical neuroimaging Article de journal Neuroscience, 181 , p. 134–49, 2011, ISSN: 1873-7544 (Electronic) 0306-4522 (Linking). |
Can imagined whole-body rotations improve vestibular compensation? Article de journal Med Hypotheses, 76 , p. 816–9, 2011, ISSN: 1532-2777 (Electronic) 0306-9877 (Linking), (6). |
The thalamocortical vestibular system in animals and humans Article de journal Brain Res Rev, 67 , p. 119–146, 2011, ISSN: 1872-6321 (Electronic) 0165-0173 (Linking), (119). |
Age-related impairment of ultrasonic vocalization in TauṖ301L mice: possible implication for progressive language disorders Article de journal PloS one, 6 (10), p. e25770, 2011, ISSN: 1932-6203. |
[Discovering a new functional neurogenic zone: the vestibular nuclei of the brainstem] Article de journal Médecine sciences: M/S, 27 (6-7), p. 605–613, 2011, ISSN: 0767-0974. |
Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage Article de journal PloS one, 6 (8), p. e22262, 2011, ISSN: 1932-6203. |
Vestibular information is necessary for maintaining metric properties of representational space: evidence from mental imagery Article de journal Neuropsychologia, 49 (11), p. 3136–3144, 2011, ISSN: 1873-3514. |
Betahistine treatment improves the recovery of static symptoms in patients with unilateral vestibular loss Article de journal Journal of clinical pharmacology, 51 (4), p. 538–548, 2011, ISSN: 1552-4604. |