Service De Neurologie Research Articles

A 3D neurons model to evaluate the neurotoxicity of harmane, a β carboline alkaloid incriminated in Essential Tremor

Event Abstract Back to Event A 3D neurons model to evaluate the neurotoxicity of harmane, a β carboline alkaloid incriminated in Essential Tremor Rania Aro1*, Alpha Diallo2, 3, Marvyn Pichueque2, 3, Mathilde Wauters4, Amandine Nachtergael1, Laurence Ris4, Pierre Duez1 and Mario Manto2, 3 1 University of Mons, Belgium 2 Free University of Brussels, Belgium 3 Service de Neurologie, Centre Hospitalier Universitaire de Charleroi, Belgium 4 Research Institute for Biosciences, University of Mons, Belgium Introduction: β-Carbolines alkaloids (βCAs) are indole alkaloids, such as harmane, that naturally occur in plants and food and are also endogenously produced in mammals and humans. Some βCAs are potent tremor inductors and exhibit neurotoxicological activities. They have been incriminated in the pathogenesis of Essential tremor (ET) as blood Harmane levels have been found to be abnormally increased in ET patients. Harmane has also been detected in post-mortem brain samples. Essential tremor (ET) is one of the most prevalent neurological diseases but, despite a high prevalence, its physiopathology remains poorly understood. There is converging evidence that both genetic and environmental factors play a role in ET pathogenesis and so the identification of involved environmental factors is a critical step towards risk reduction through the implementation of prevention strategies or interventional studies. 2D cell cultures do not represent the real cell environment where cells spatially and chemically interact; their lack in predictivity increases the cost and failure rate of clinical trials, especially in neurosciences. Recently, 3D cell cultures have received much attention, as these are closer to tissues models, although their main challenges reside in end-point measurements. Methods: We propose the use of a 3D neural spheroid cultures ("mini-brains") in vitro model to assess the neurotoxic effects of harmane. We have generated a model of 3D spheroids from embryonic mouse cortical neurons using micro-molded agarose wells. After exposure to harmane at increasing concentrations of 50, 100, 250 µM, a resazurin assay was performed to measure cell viability and a highly sensitive fluorometric method, based on the oxidation of di-chlorodihydrofluorescein DCFH, was used to measure eventually induced reactive oxygen species (ROS). Results: Hydrogel microwells facilitated the assembly of spheroids containing neurons and glia into a complex 3D structures and prevented the agglomeration of spheroids. Exposure to harmane induced a cytotoxicity in 3D neural spheroids that was correlated with harmane concentrations, with a viability down to 24 % at 250 µM. On the other hand, lower levels of oxidative stress were detected as the harmane concentration increased, although the effect was limited in time. Conclusions: We demonstrated our ability to produce a 3D culture using simple materials and routine laboratory equipment. Despite high challenges related to 3D cultures and data acquisition, this 3D neural spheroid model mimics a neuronal microenvironment, allowing a fine study of neurodegenerative disorder pathologies and the effect of chemicals on the brain. The viability and oxidative stress data support so far a dual role of harmane, as both neurotoxic and neuroprotective agent. Further studies are required to elucidate its biological activities and their eventual relationship with the ET disorder. Acknowledgements This research is in part funded through a FMRH grant and a Kangaroo grant from the UMONS Health Institute .

Multiple sclerosis, emotions and social cognition

A. Tourbah*, N. Ehrle, N. Henry, S. Bakchine, M.P. Chaunu,M. MontreuilCHRU de Reims, service de neurologie, hopital Maison-Blanche, 45, rueCognacq Jay, URCA LPN UE 2027, Paris VIII, 51092 Reims, France*Corresponding author.E-mail address: atourbah@chu-reims.frKeywords: Multiple sclerosis; Alexithymia; Theory of mind; Emotion;CognitionEmotional processes are governed by the areas and neural systems that can beexplored MRI (amygdala, orbitofrontal cortex, cingulate cortex, insula). It isnowpossibletoexplorebyMRI,usingtechniquesbasedonfunctionalMRIanddiffusion tensor including (anatomical and functional connectivity).These processes seem disturbed in MS. Indeed, the motor and neurosensorydisabilityisassociatedwithcognitivedisorders,mooddisorders,andemotionaland socio-cognitive deficit.Emotions play a critical role in the organization of social processes in differentareas of cognition (memory, attention decision). Besides alexithymia (difficultyverbalizing emotional experiences, fantasy poverty), social cognition is the skillsetthatallows ustointerpret and predictthebehaviorofothers.Their disruptioninvolvedinthesepatientswithbehavioralproblemsandsocialadjustment.Toolstoexplorethesedisturbances,includingthestudyoffacialexpressions(perceptionof primary emotions), and theory of mind (attribution of thoughts to others).Their management is insufficient. The detection and treatment of emotionaldisorders (in addition to cognitive impairment, fatigue and mood disorders) isdesirable for these patients to maintain social and family life, and improvequality of life. It has not been shown that treatments, currently used in MS, areeffective in this area. The establishment of workshops rehabilitation would beuseful.Further readingBanati M, Sandor, J., Mike, A., Illes, E., Bors, L., Feldmann, A., Herold, R. &Illes Z. (2009). Social cognition and Theory of Mind in patients withrelapsing-remitting multiple sclerosis. European Journal of Neurology, 17(3),426-433.Henry A, Tourbah A, Chaunu MP, Rumbach L,Montreuil M, Bakchine S.Social Cognition Impairments in Relapsing-Remitting Multiple Sclerosis. J IntNeuropsychol Soc (2011), 17, 1122-1131.http://dx.doi.org/10.1016/j.rehab.2013.07.906CO04-002-e

The status of rotigotine as a safe and effective alternative in the treatment of restless legs syndrome

Eric Frenette CHUS a/s Service de Neurologie, 3001 12e Avenue Nord, Sherbrooke, QC, J1H 5N4, Canada Tel +1 819 346 1110 Ext 14589 Email eric.frenette@usherbrooke.ca Abstract: Restless legs syndrome (RLS) is characterized by an urge to move the legs that occurs mainly with inactivity, and it is relieved by movement and is usually worse by the end of the day. It is highly prevalent, affecting 1.9% to 4.5% of the population, and although its etiology is uncertain, genetic factors seem to be involved. When symptoms are severe enough to warrant chronic therapy, dopamine receptor agonists are to be considered for initial treatment. Rotigotine, the most recently developed drug in this category, is the only one available for transdermal delivery in RLS. It was initially designed for the treatment of Parkinson’s disease. The US Food and Drug Administration approved its use in cases of moderate to severe RLS in April 2012. Its efficacy has been well established in randomized placebo-controlled trials, as it appears to be especially useful in patients with daily symptoms. The most commonly reported side effect is local skin reaction. Complications such as augmentation, somnolence, or compulsive behavior may happen, although they seldom occur. The American Academy of Sleep Medicine clinical practice guideline recommends a “Guideline Level” for rotigotine, and European RLS guidelines provide a “level A” recommendation for short-term therapy; it also was the only dopaminergic agonist considered to be effective for the long-term management of RLS.

New hands at the helm

It is with great regret that I have to say good-bye to my CoChief Editor Professor Gerard Said, who after 3 years has decided to step down. His successors, of whom there are two, are Michael Strupp and Massimo Filippi. Gerard took on this role with myself and Thomas Brandt back in January 2009, and since then the journal has continued to grow in terms of the number of submissions it receives and its impact factor, in no small part because of Gerard’s skills and his well-established and leading role in the European Neurological Society (ENS), to which the journal is linked. Gerard qualified in neurology from the medical school of the Salpetriere back in 1971 and since then has become an international academic neurologist of great repute as well as being highly influential in many different areas of neurological practice and training, both nationally and internationally. Apart from being the Professor of Neurology and Chief of Service de Neurologie at the Centre Hospitalier Universitaire de Bicetre, Universite Paris-Sud from 1987 to 2007, he was also a co-founder of the ENS in 1986 with the late P.K. Thomas and Anita Harding. This new society was born out of a sense that there was nothing equivalent to the American Academy of Neurology in Europe. Gerard became the first Secretary General of the society until 2007 and has been instrumental in organising all of their yearly congresses. He became President of the ENS in 2010. His main field of investigation has been in the area of peripheral neuropathies, where he has made many seminal contributions, and he is perhaps best known for his work on diabetic and vasculitic neuropathy. However, his work extends to many aspects of the peripheral nervous system, with influential work on infectious causes of peripheral nerve dysfunction such as HIV-associated neuropathies. This work has led not only to a better description and recognition of these conditions, but also to better investigation and treatment. This ability to master the whole spectrum of peripheral nerve disease has led to him taking an international role in this field of neurology. He has been Director of the Research Group on Neuromuscular Disorders of the World Federation of Neurology, and between 1998 and 2000 he was also President of the Peripheral Nerve Society (PNS). During his 3 years at the helm of the Journal of Neurology Gerard has been instrumental in speeding up the review process, in bringing in new initiatives, and in R. A. Barker (&) Cambridge Centre for Brain Repair, University of Cambridge, The E.D. Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK e-mail: rab46@cam.ac.uk

Response to Letter by Blackburn et al Regarding Article, “Is the Montreal Cognitive Assessment Superior to the Mini-Mental State Examination to Detect Poststroke Cognitive Impairment? A Study With Neuropsychological Evaluation”

HomeStrokeVol. 42, No. 11Response to Letter by Blackburn et al Regarding Article, “Is the Montreal Cognitive Assessment Superior to the Mini-Mental State Examination to Detect Poststroke Cognitive Impairment? A Study With Neuropsychological Evaluation” Free AccessReplyPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReplyPDF/EPUBResponse to Letter by Blackburn et al Regarding Article, “Is the Montreal Cognitive Assessment Superior to the Mini-Mental State Examination to Detect Poststroke Cognitive Impairment? A Study With Neuropsychological Evaluation” Olivier Godefroy, MD, PhD, Jean Marc Bugnicourt, MD and Andreas Fickl, MD Olivier GodefroyOlivier Godefroy Service de Neurologie CHU Nord Amiens, France (Godefroy,Bugnicourt,Fickl) Search for more papers by this author , Jean Marc BugnicourtJean Marc Bugnicourt Service de Neurologie CHU Nord Amiens, France (Godefroy,Bugnicourt,Fickl) Search for more papers by this author and Andreas FicklAndreas Fickl Service de Neurologie CHU Nord Amiens, France (Godefroy,Bugnicourt,Fickl) Search for more papers by this author Originally published22 Sep 2011https://doi.org/10.1161/STROKEAHA.111.630368Stroke. 2011;42:e583Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2011: Previous Version 1 Response:We thank Blackburn et al for their interesting comments on screening tests for poststroke cognitive impairment. Given the frequency and impact of poststroke cognitive impairment, choosing the best possible screening test is important. In view of the MMSE score's poor sensitivity to vascular cognitive impairment and our recent results,1 Blackburn et al suggest that the Montreal Cognitive Assessment (MoCA) should be used instead of the MMSE, with a cutoff ≤23. Although we agree with some of Blackburn et al's points, the currently available evidence (including our own study) does not fully support their position. First, our study supported the moderate sensitivity (0.66) of MMSE when recommended cutoffs are used.1 However, sensitivity improved using cut-off after adjustment of the score for education level (Table 21). Second, Blackburn et al indicate that use of a cutoff ≤23 for the MoCA yielded a sensitivity of 0.84 and a specificity of 0.81 as indicated in Table 3.1 We wish to emphasize that this cut-off does not concern the raw MoCA score, only a specific adjustment of the score for age and education level (Table 31). Third, Blackburn et al indicate that a test with sensitivity and specificity >0.8 meets the criterion for being a good screening tool.The criterion for being an optimal screening test is a critical point. In the article, we provided 2 cut-off values for each test, either to optimize the trade-off between sensitivity and specificity (adjusted MMSE, ≤24; adjusted MoCA, ≤20) or to minimize the false-negative rate (MMSE adjusted, ≤29; MoCA adjusted, ≤26). This allows the reader to choose the test and cut-off according to his/her objective. We agree with the idea that cognitive impairment should be systematically screened for within 6 months of a stroke. Given that the primary objective of stroke care is not the systematic analysis of cognitive and behavioral complaints, the screening tool should minimize the false-negative rate and the likelihood ratio of a negative test (LRN).2 This is achieved after adjustment of the score for age and educational level using our proposed cut-offs for the MMSE (MMSE adjusted, ≤29; false-negative rate, 1 of 62 [ie, 1.6%]; LRN, 0.097) and the MoCA (MoCA adjusted, ≤26; false-negative rate, 3.2%; LRN, 0.06). Conversely, other cut-offs provide higher false-negative rates (MMSE adjusted, ≤24; false-negative rate, 31%; LRN, 0.31; MoCA adjusted, ≤20; false-negative rate, 31%; LRN, 0.36). A high false-negative rate is also observed for the cut-off proposed by Blackburn et al (MoCA adjusted, ≤23; false-negative, 13%; LRN, 0.19). Lastly, the use of a cut-off that minimizes false-negatives would result in cognitive assessment of half the screened patients1 (and not in 80% as suggested by Blackburn et al). The ongoing GRECOG-VASC study (ClinicalTrials.gov identifier: NCT01339195) will provide norms for the MoCA in French-speaking subjects and will examine the ability of these 2 screening tests to predict cognitive impairment at 6 months poststroke.Olivier Godefroy, MD, PhDJean Marc Bugnicourt, MDAndreas Fickl, MD Service de Neurologie CHU Nord Amiens, FranceDisclosuresNone.FootnotesStroke welcomes Letters to the Editor and will publish them, if suitable, as space permits. Letters must reference a Stroke published-ahead-of-print article or an article printed within the past 3 weeks. The maximum length is 750 words including no more than 5 references and 3 authors. Please submit letters typed double-spaced. Letters may be shortened or edited. Include a completed copyright transfer agreement form (available online at http://stroke.ahajournals.org and http://submit-stroke.ahajournals.org).

Cerebellar Nuclei: Key Roles for Strategically Located Structures

With the exception of vestibular information, cerebellar nuclei represent the unique source of output of the cerebellar circuitry. The fastigial (FN), globose/emboliform (interpositus, IN), and dentate (DN) nuclei receive inhibitory GABAergic signals from Purkinje neurons and send back fibers to the cerebellar cortex. The numerous GABAA inhibitory synapses between cerebellar cortex and cerebellar nuclei allow responses to high-frequency Purkinje cell firing [1]. Cerebellar nuclei receive excitatory collaterals of mossy fibers and climbing fibers, especially via AMPA and NMDA receptors [2]. A subset of small neurons in cerebellar nuclei project to the inferior olivary complex, providing a feedback to the inferior olive. Cerebellar nuclei thus integrate the converging excitatory and inhibitory signals to provide the final output of the cerebellar circuits. Each cerebellar nucleus has a separate somatotopic representation of the body [3]. The projections to different cerebral cortical areas originate from distinct areas of cerebellar nuclei. In particular, the DN is spatially divided into a motor and nonmotor zone, with a closed loop from the nucleus to the cerebral cortex and back to the nucleus. Cerebellar nuclei control differentially the medial and lateral motor systems and their functions [4]. The vestibular and FN are concerned with the control of eye movements, control of head orientation, stance, and gait. FN can be functionally divided into rostral and caudal components [4, 5]. The rostral portion is involved in the control of somatic musculature, head orientation, and eye-gaze shifts [4]. The caudal FN plays key roles in saccade generation and smooth pursuit [6]. The IN is particularly active during the modulation of various reflexes and sensory feedback [7]. The eyeblink responses are typically associated with a modulation of activity in behaving animals [8]. The intermediate cortex and the IN fire in relation to the antagonist muscle group [9, 10], in agreement with a role in damping the limb oscillations and compensation of errors [11]. The IN participates in the excitability of the stretch reflexes [12]. The DN is especially concerned with voluntary movements of the extremities, including reaching and grasping. Dentate neurons preferentially fire at the onset of movement triggered by mental associations [4]. An influential theory is that cerebellar nuclei constitute temporal pattern generators that can contribute to the precise temporal control of motor or cognitive events [13, 14]. The plasticity of Purkinje neurons–cerebellar nuclei synapses is based upon synaptically driven changes in excitability and LTP/LTD [15–17]. In conjunction with the LTP/LTD in cerebellar cortex and the adaptations occurring in mossy/ climbing fibers, such plasticity allows for reshaping of patterns of activities in cerebellar nuclei. On the basis of GABA decarboxylase isoform 67 (GAD67) expression and electrophysiological properties, three types of cerebellar nuclei neurons have been described [18]: the large non-GABAergic neurons (“GADnL”; putatively corresponding to the glutamatergic projection neurons) and two classes of smaller neurons, one M. Manto :N. Oulad Ben Taib Service de Neurologie et Neurochirurgie, ULB Erasme, Brussels, Belgium

Making Similarities and Conceptualizing are Two Prefrontal Distinct Functions Serving Categorization

Event Abstract Back to Event Making Similarities and Conceptualizing are Two Prefrontal Distinct Functions Serving Categorization B. Dubois1, 2, B. Garcin1, 3*, R. Levy1, 3, B. Oliviero1 and E. Volle1 1 INSERM UMRS 975, Institut du cerveau et de la moelle épiniére (ICM), France 2 hôpital Pitié-Salpêtrière, AP-HP Service deneurologie, France 3 hôpital Saint-Antoine, AP-HP Service de neurologie, France While performing categorization tasks, some patients with frontal lobe syndrome could not indicate the physical similarities between real-life objects, whereas others could not conceptualize the abstract (or semantic) link that binds these elements. This clinical dissociation raises the question of whether making similarities and conceptualizing are two distinct processes involving separate areas of the prefrontal cortex (PFC). To test these hypotheses, 20 healthy human subjects performed an fMRI experiment combined with an experimental cognitive paradigm that allowed us to study separately the neural basis of similarities and conceptualization. This study shows that making similarities involves bilaterally the rostral ventrolateral prefrontal regions (BA 11/47), whereas conceptualization activates different areas located in the left dorsolateral and ventrolateral PFC (BA 8/9/10/44/45), without overlap between activation dedicated to these two processes and no significant interaction between them. The results of this study suggest that making similarities and conceptualizing are two independent processes relying on different prefrontal areas. These results will be discussed in terms of their implications to understand the role of the PFC in behavioral integration as well as their potential impact to understand the clinical syndrome that occurs after damage to different parts of the frontal lobes. Conference: The 20th Annual Rotman Research Institute Conference, The frontal lobes, Toronto, Canada, 22 Mar - 26 Mar, 2010. Presentation Type: Poster Presentation Topic: Cognitive Neuroscience Citation: Dubois B, Garcin B, Levy R, Oliviero B and Volle E (2010). Making Similarities and Conceptualizing are Two Prefrontal Distinct Functions Serving Categorization. Conference Abstract: The 20th Annual Rotman Research Institute Conference, The frontal lobes. doi: 10.3389/conf.fnins.2010.14.00106 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 29 Jun 2010; Published Online: 29 Jun 2010. * Correspondence: B. Garcin, INSERM UMRS 975, Institut du cerveau et de la moelle épiniére (ICM), Paris, France, beagarcin@msn.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers B. Dubois B. Garcin R. Levy B. Oliviero E. Volle Google B. Dubois B. Garcin R. Levy B. Oliviero E. Volle Google Scholar B. Dubois B. Garcin R. Levy B. Oliviero E. Volle PubMed B. Dubois B. Garcin R. Levy B. Oliviero E. Volle Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Tuesday July 4, 2006 Tuesday July 4, 2006 7:30-9:00 Hall 1 Orphan Drug Symposium

Abstract 1 M. Baulac ( 1 Service de Neurologie, Hopital Pitie-Salpetriere, Paris, France ) Although epilepsy is one of the commonest neurological disorders, certain epileptic syndromes or diseases are nonetheless fulfilling all the criteria, in terms of epidemiology and severity, for being qualified as rare diseases. These epileptic conditions indeed are distinct entities, affecting no more than 5 in 10,000 persons in Europe, carrying a risk of chronic impairment, severe debilitation, and mortality, and there is a lack of specific treatments with durable effects on the seizures and the neuropsychological disorders. Most of the epileptic encephalopathies can be qualified as rare diseases. They include Ohtahara syndrome / early myoclonic encephalopathy, migrating partial seizures in infancy, West syndrome, Dravet syndrome or severe myoclonic epilepsy in Infancy (1/30,000), Lennox-Gastaut syndrome (2/10,000), Landau-Kleffner syndrome, continuous spike-wave during sleep, etc… In these specific conditions, the intense ictal and interictal epileptic activity contributes to the progressive disturbance in brain function. These epileptic encephalopathies can themselves be caused by rare mutations or other rare diseases, for instance tuberous sclerosis in West syndrome. Orphan drugs, which are still in development, have been designated by the EMEA for the Dravet syndrome (stiripentol) and for the Lennox-Gastaut syndrome (rufinamide). In other situations, epilepsy is the predominant clinical expression of a disease of genetic, metabolic or inflammatory origin, which is responsible for progressive brain damage. Progressive myoclonic epilepsies (less than 1/20,000) for which brivaracetam was recently designated, and Rasmussen encephalopathy (approximately 1 case per big center per year) are good examples. It is very important for our patients and their families to ensure that these conditions are well acknowledged as rare diseases, and that they can benefit from the various governmental and EU incentives dedicated to specific research and Orphan drugs development.

Differential Effects of L-Dopa and Subthalamic Stimulation on Depressive Symptoms and Hedonic Tone in Parkinson's Disease

Differential Effects of L-Dopa and Subthalamic Stimulation on Depressive Symptoms and Hedonic Tone in Parkinson's Disease

Familial oculoparetic torticolis

European Journal of NeurologyVolume 13, Issue 8 p. e3-e4 Familial oculoparetic torticolis E. Carrera, E. Carrera Departments of NeurologySearch for more papers by this authorJ. Bogousslavsky, J. Bogousslavsky Departments of NeurologySearch for more papers by this authorT. Kuntzer, T. Kuntzer Departments of NeurologySearch for more papers by this authorP. Maeder, P. Maeder Departments of NeurologySearch for more papers by this authorJ. Ghika, J. Ghika Departments of NeurologySearch for more papers by this author E. Carrera, E. Carrera Departments of NeurologySearch for more papers by this authorJ. Bogousslavsky, J. Bogousslavsky Departments of NeurologySearch for more papers by this authorT. Kuntzer, T. Kuntzer Departments of NeurologySearch for more papers by this authorP. Maeder, P. Maeder Departments of NeurologySearch for more papers by this authorJ. Ghika, J. Ghika Departments of NeurologySearch for more papers by this author First published: 20 July 2006 https://doi.org/10.1111/j.1468-1331.2006.01248.x E. Carrera, MD, Service de Neurologie, CHUV BH 07, CH – 1011 Lausanne, Switzerland (e-mail: emmanuel.carrera@chuv.hospvd.ch). Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume13, Issue8August 2006Pages e3-e4 RelatedInformation

Carotid Endarterectomy Versus Stenting: An International Perspective

To the Editor: With interest we read the comment of Hobson et al entitled “Carotid Artery Stenting and the Recruitment Challenges in a clinical trial.”1 Although we completely share the concerns of the authors regarding slow recruitment into the CREST Trial, constantly growing use of carotid stenting in symptomatic patients outside of protocols, and the lack of evidence in this area, we cannot agree with the perception that it is mostly up to CREST to solve the problems. The authors mention shortly that larger clinical trials “are currently underway in North America and Europe.” With reference 10 they cite the CAVATAS trial that finished recruitment long ago. They state that “recruitment into these trials will also be slow and the data may not be available for the next 2 to 3 years.” As the principal investigators of 3 European Trials, we would …

Small fiber involvement in peripheral neuropathies

Department of Neurology, Bicêtre Hospital, Le Kremlin Bicêtre, France Correspondence to Dr Gérard Said, Service de Neurologie, Hôpital de Bicêtre, 94275 Le Kremlin Bicêtre, France Tel: +33 1 45212628; fax: +33 1 45212853; e-mail: [email protected]

Response

Response

Abstracts of literature

Abstracts of literature

Abstracts of literature

Abstracts of literature

Vesicourethral Dysfunction and Urodynamic Findings in Multiple Sclerosis: A Study of 149 Cases

Vesicourethral Dysfunction and Urodynamic Findings in Multiple Sclerosis: A Study of 149 Cases

Abstracts of Literature

Abstracts of Literature

Unilateral femoral neuropathy (a reply)

Muscle & NerveVolume 21, Issue 1 p. 127-127 Letter to the Editor Unilateral femoral neuropathy (a reply) Thierry Kuntzer MD, Corresponding Author Thierry Kuntzer MD Service de neurologie, CHUV-07, Lausanne, 1011 SwitzerlandService de neurologie, CHUV-07, Lausanne, 1011 SwitzerlandSearch for more papers by this author Thierry Kuntzer MD, Corresponding Author Thierry Kuntzer MD Service de neurologie, CHUV-07, Lausanne, 1011 SwitzerlandService de neurologie, CHUV-07, Lausanne, 1011 SwitzerlandSearch for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1097-4598(199801)21:1<127::AID-MUS20>3.0.CO;2-%23AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume21, Issue1January 1998Pages 127-127 RelatedInformation

Genetics of Friedreich Ataxia

Genotype-phenotype correlations in a group of 100 patients with typical Friedreich ataxia (FRDA), and in three smaller clinically atypical groups (Arcadian FRDA, late-onset FRDA (LOFA), and FRDA with retained reflexes (FARR)), were studied at the Centre de Recherche Louis-Charles Simard, Service de Genetique Medicale, Service de Neurologie, Hopital Sainte-Justine, Departments of Genetics and Medicine, McGill University, Montreal General Hospital, and other centers.

Machado-Joseph Disease

The frequency, and clinical, molecular, and neuropathological features of spinocerebellar ataxia 3 (SCA3) and Machado-Joseph disease (MJD) in 125 autosomal dominant cerebellar ataxia (ADCA) families were analyzed at the Service de Neuropathologie, Hopital de la Salpetriere, Paris, and Service de Neurologie, Hopital de Haut Leveque, Pessac, France; and Service de Neurologie, Hopital des Specialites, Rabat, Morocco.