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Annals of Neurology: Volume 91, Number 2, February 2022
doi : 10.1002/ana.26106
Volume 91, Issue 2 p. C1-C1
An illustration of lesion network mapping of blindsight-negative versus blindsight. This begins with representative lesion locations from a blindsight and blindsight-negative patient. Lesions were consolidated into a single hemisphere for analysis. Connectivity between each lesion location and the rest of the brain was computed using a normative database of resting state functional connectivity from 1000 healthy subjects. Pictured are the connectivity patterns derived from the two representative lesion locations. Connectivity differences between lesion locations from blindsight-negative (n=35) versus blindsight patients (n=34) were identified using a two-sample, voxelwise t-test within a mask of regions previously implicated in blindsight (dark grey). Lesions in blindsight-negative patients showed greater functional connectivity to the medial pulvinar (pulvinar in blue outline) compared to lesions in blindsight patients. See paper in this issue by Kletenik et al. (pp. 217–224).
Adaptive Platform Trials to Transform Amyotrophic Lateral Sclerosis Therapy Development
Sabrina Paganoni MD, PhD,James D. Berry MD, MPH,Melanie Quintana PhD,Eric Macklin PhD,Benjamin R. Saville PhD,Michelle A. Detry PhD,Marianne Chase BA,Alexander V. Sherman MSc,Hong Yu MS,Kristin Drake MBA,Jinsy Andrews MD,Jeremy Shefner MD, PhD,Lori B. Chibnik PhD, MPH,Matteo Vestrucci PhD,Merit E. Cudkowicz MD, MSc,for the Healey ALS Platform Trial Study Group
doi : 10.1002/ana.26285
Volume 91, Issue 2 p. 165-175
Current therapeutic development in amyotrophic lateral sclerosis (ALS) relies on individual randomized clinical trials to test a specific investigational product in a single patient population. This approach has intrinsic limitations, including cost, time, and lack of flexibility. Adaptive platform trials represent a novel approach to investigate several interventions for a single disease in a continuous manner. Already in use in oncology, this approach is now being employed more often in neurology. Here, we describe a newly launched platform trial for ALS. The Healey ALS Platform Trial is testing multiple investigational products concurrently in people with ALS, with the goal of rapidly identifying novel treatments, biomarkers, and trial endpoints. ANN NEUROL 2022;91:165–175
ANA Podcasts & Webinars: Neuromodulation in Epilepsy
Rohit R. Das MD,Adeline L. Goss MD,Megan B. Richie MD,Vikram R. Rao MD, PhD
doi : 10.1002/ana.26276
Volume 91, Issue 2 p. 176-177
Human Oligodendrocyte Myelination Potential; Relation to Age and Differentiation
Julia Xiao Xuan Luo MSc,Qiao-Ling Cui MD, PhD,Moein Yaqubi PhD,Jeffery A. Hall MD,Roy Dudley MD, PhD,Myriam Srour MD, PhD,Nassima Addour PhD,Hélène Jamann PhD,Catherine Larochelle MD, PhD,Manon Blain,Luke M. Healy PhD,Jo Anne Stratton PhD,Joshua A. Sonnen MD,Timothy E. Kennedy PhD,Jack P. Antel MD
doi : 10.1002/ana.26288
Volume 91, Issue 2 p. 178-191
Myelin regeneration in the human central nervous system relies on progenitor cells within the tissue parenchyma, with possible contribution from previously myelinating oligodendrocytes (OLs). In multiple sclerosis, a demyelinating disorder, variables affecting remyelination efficiency include age, severity of initial injury, and progenitor cell properties. Our aim was to investigate the effects of age and differentiation on the myelination potential of human OL lineage cells.
Subcortical Volumes as Early Predictors of Fatigue in Multiple Sclerosis
Vinzenz Fleischer MD,Dumitru Ciolac MD,Gabriel Gonzalez-Escamilla PhD,Matthias Grothe MD,Sebastian Strauss MD,Lara S. Molina Galindo MD,Angela Radetz PhD,Anke Salmen MD,Carsten Lukas MD,Luisa Klotz MD,Sven G. Meuth MD, PhD,Antonios Bayas MD,Friedemann Paul MD,Hans-Peter Hartung MD,Christoph Heesen MD,Martin Stangel MD,Brigitte Wildemann MD,Florian Then Bergh MD,Björn Tackenberg MD,Tania Kümpfel MD,Uwe K. Zettl MD,Matthias Knop MD,Hayrettin Tumani MD,Heinz Wiendl MD,Ralf Gold MD,Stefan Bittner MD,Frauke Zipp MD,Sergiu Groppa MD,Muthuraman Muthuraman PhD,the German Competence Network Multiple Sclerosis (KKNMS)
doi : 10.1002/ana.26290
Volume 91, Issue 2 p. 192-202
Fatigue is a frequent and severe symptom in multiple sclerosis (MS), but its pathophysiological origin remains incompletely understood. We aimed to examine the predictive value of subcortical gray matter volumes for fatigue severity at disease onset and after 4?years by applying structural equation modeling (SEM).
Aerobic Exercise Alters Brain Function and Structure in Parkinson's Disease: A Randomized Controlled Trial
Martin E. Johansson MSc,Ian G. M. Cameron PhD,Nicolien M. Van der Kolk MD, PhD,Nienke M. de Vries PhD,Eva Klimars MSc,Ivan Toni PhD,Bastiaan R. Bloem MD, PhD,Rick C. Helmich MD, PhD
doi : 10.1002/ana.26291
Volume 91, Issue 2 p. 203-216
Randomized clinical trials have shown that aerobic exercise attenuates motor symptom progression in Parkinson's disease, but the underlying neural mechanisms are unclear. Here, we investigated how aerobic exercise influences disease-related functional and structural changes in the corticostriatal sensorimotor network, which is involved in the emergence of motor deficits in Parkinson's disease. Additionally, we explored effects of aerobic exercise on tissue integrity of the substantia nigra, and on behavioral and cerebral indices of cognitive control.
Network Localization of Unconscious Visual Perception in Blindsight
Isaiah Kletenik MD,Michael A. Ferguson PhD,James R. Bateman MD, MPH,Alexander L. Cohen MD, PhD,Christopher Lin BS,Aaron Tetreault BS,Victoria S. Pelak MD,Clark Alan Anderson MD,Sashank Prasad MD,Richard Ryan Darby MD,Michael D. Fox MD, PhD
doi : 10.1002/ana.26292
Volume 91, Issue 2 p. 217-224
Blindsight is a disorder where brain injury causes loss of conscious but not unconscious visual perception. Prior studies have produced conflicting results regarding the neuroanatomical pathways involved in this unconscious perception.
Variants in Mitochondrial ATP Synthase Cause Variable Neurologic Phenotypes
Michael Zech MD,Robert Kopajtich MSc,Katja Steinbrücker MD,Céline Bris PhD,Naig Gueguen PhD,René G. Feichtinger PhD,Melanie T. Achleitner MSc,Neslihan Duzkale MD,Maximilien Périvier MD,Johannes Koch MD,Harald Engelhardt MD,Peter Freisinger MD,Matias Wagner MD,Theresa Brunet MD,Riccardo Berutti PhD,Dmitrii Smirnov MSc,Tharsini Navaratnarajah MSc,Richard J.T. Rodenburg PhD,Lynn S Pais MS,Christina Austin-Tse PhD,Melanie O'Leary MS,Sylvia Boesch MD,Robert Jech MD,Somayeh Bakhtiari PhD,Sheng Chih Jin PhD,Friederike Wilbert MD,Michael C Kruer MD,Saskia B. Wortmann MD,Matthias Eckenweiler MD,Johannes A. Mayr MD,Felix Distelmaier MD,Robert Steinfeld MD,Juliane Winkelmann MD,Holger Prokisch PhD
doi : 10.1002/ana.26293
Volume 91, Issue 2 p. 225-237
ATP synthase (ATPase) is responsible for the majority of ATP production. Nevertheless, disease phenotypes associated with mutations in ATPase subunits are extremely rare. We aimed at expanding the spectrum of ATPase-related diseases.
Induction of Human Motor Cortex Plasticity by Theta Burst Transcranial Ultrasound Stimulation
Ke Zeng PhD,Ghazaleh Darmani PhD,Anton Fomenko MD,Xue Xia PhD,Stephanie Tran MSc,Jean-François Nankoo PhD,Yazan Shamli Oghli BSc,Yanqiu Wang PhD,Andres M. Lozano MD, PhD, FRCSC,Robert Chen MBBChir, MSc, FRCPC
doi : 10.1002/ana.26294
Volume 91, Issue 2 p. 238-252
Transcranial ultrasound stimulation (TUS) is a promising noninvasive brain stimulation technique with advantages of high spatial precision and ability to target deep brain regions. This study aimed to develop a TUS protocol to effectively induce brain plasticity in human subjects.
DBS of Thalamic Centromedian Nucleus for Lennox–Gastaut Syndrome (ESTEL Trial)
Linda J. Dalic MBBS,Aaron E. L. Warren PhD,Kristian J. Bulluss PhD,Wesley Thevathasan DPhil,Annie Roten BAppSci,Leonid Churilov PhD,John S. Archer PhD
doi : 10.1002/ana.26280
Volume 91, Issue 2 p. 253-267
Prior uncontrolled studies have reported seizure reductions following deep brain stimulation (DBS) in patients with Lennox–Gastaut syndrome (LGS), but evidence from randomized controlled studies is lacking. We aimed to formally assess the efficacy and safety of DBS to the centromedian thalamic nucleus (CM) for the treatment of LGS.
Spinal Cord Atrophy Predicts Progressive Disease in Relapsing Multiple Sclerosis
Antje Bischof MD,Nico Papinutto PhD,Anisha Keshavan PhD,Anand Rajesh BS,Gina Kirkish MS,Xinheng Zhang MS,Jacob M. Mallott MS,Carlo Asteggiano MD,Simone Sacco MD,Tristan J. Gundel BS,Chao Zhao MS,William A. Stern RT(MR),Eduardo Caverzasi MD,Yifan Zhou BA,Refujia Gomez BS,Nicholas R. Ragan BS,Adam Santaniello BSc,Alyssa H. Zhu MS,Jeremy Juwono BS,Carolyn J. Bevan MD,Riley M. Bove MD,Elizabeth Crabtree MD,Jeffrey M. Gelfand MD,Douglas S. Goodin MD,Jennifer S. Graves MD,Ari J. Green MD,Jorge R. Oksenberg PhD,Emmanuelle Waubant MD,Michael R. Wilson MD,Scott S. Zamvil MD,University of California, San Francisco MS-EPIC Team,Bruce A. C. Cree MD,Stephen L. Hauser MD,Roland G. Henry PhD
doi : 10.1002/ana.26281
Volume 91, Issue 2 p. 268-281
A major challenge in multiple sclerosis (MS) research is the understanding of silent progression and Progressive MS. Using a novel method to accurately capture upper cervical cord area from legacy brain MRI scans we aimed to study the role of spinal cord and brain atrophy for silent progression and conversion to secondary progressive disease (SPMS).
Reduced Numbers of Corticotropin-Releasing Hormone Neurons in Narcolepsy Type 1
Ling Shan PhD,Rawien Balesar MSc,Dick F. Swaab MD, PhD,Gert Jan Lammers MD, PhD,Rolf Fronczek MD, PhD
doi : 10.1002/ana.26300
Volume 91, Issue 2 p. 282-288
Narcolepsy type 1 (NT1) is a chronic sleep disorder correlated with loss of hypocretin(orexin). In NT1 post-mortem brains, we observed 88% reduction in corticotropin-releasing hormone (CRH)-positive neurons in the paraventricular nucleus (PVN) and significantly less CRH-positive fibers in the median eminence, whereas CRH-neurons in the locus coeruleus and thalamus, and other PVN neuronal populations were spared: that is, vasopressin, oxytocin, tyrosine hydroxylase, and thyrotropin releasing hormone-expressing neurons. Other hypothalamic cell groups, that is, the suprachiasmatic, ventrolateral preoptic, infundibular, and supraoptic nuclei and nucleus basalis of Meynert, were unaffected. The surprising selective decrease in CRH-neurons provide novel targets for diagnostics and therapeutic interventions. ANN NEUROL 2022;91:282–288
Insular Stimulation Produces Mental Clarity and Bliss
Umberto Nencha MD,Laurent Spinelli PhD,Serge Vulliemoz MD, PhD,Margitta Seeck MD,Fabienne Picard MD
doi : 10.1002/ana.26282
Volume 91, Issue 2 p. 289-292
For the first time, an ecstatic aura has been evoked through the electrical stimulation of the dorsal anterior insula during presurgical invasive intracerebral monitoring in a patient who did not suffer from an ecstatic form of epilepsy. This case provides more evidence that the anterior insula is the major generator of such a mystical-type experience even in individuals with no underlying brain network changes related to a preexisting ecstatic epilepsy. ANN NEUROL 2022;91:289–292
Filum Terminale Hemangioblastoma with Four Categories of Lesions
Shixiong Lei MD,Yan Hu MD,Meng Wang MD,Fuyou Guo MD
doi : 10.1002/ana.26271
Volume 91, Issue 2 p. 293-294
The Neural Networks Underlying the Illusion of Time Dilation
Muhammad Mubbashir Sheikh MD,Mohamad Z. Koubeissi MD,Dennis D. Spencer MD,Rafeed Alkawadri MD
doi : 10.1002/ana.26277
Volume 91, Issue 2 p. 295-297
A Recurrent KPNA3 Missense Variant Causing Infantile Pure Spastic Paraplegia
Jonathan De Winter MD,Liedewei Van de Vondel MSc,Stephan Züchner MD, PhD,Els Ortibus MD, PhD,Jonathan Baets MD, PhD
doi : 10.1002/ana.26297
Volume 91, Issue 2 p. 298-299
Investigating the Immunopathogenic Mechanisms Underlying MOGAD
Jennifer A. McCombe MD,Eoin P. Flanagan MD,John J. Chen MD, PhD,Anastasia Zekeridou MD, PhD,Claudia F. Lucchinetti MD,Sean J. Pittock MD
doi : 10.1002/ana.26279
Volume 91, Issue 2 p. 299-300
Reply to “Investigating the Immunopathogenic Mechanisms Underlying MOGAD”
Christian W. Keller MD, PhD,Joseph A. Lopez BSc,Eva-Maria Wendel MD,Sudarshini Ramanathan MD, PhD,Catharina C. Gross PhD,Luisa Klotz MD,Markus Reindl PhD,Russell C. Dale MD,Heinz Wiendl MD,Kevin Rostásy MD,Fabienne Brilot PhD,Jan D. Lünemann MD
doi : 10.1002/ana.26278
Volume 91, Issue 2 p. 300-301
German Neurology in 1982: Society in Transition
Rüdiger J. Seitz MD
doi : 10.1002/ana.26283
Volume 91, Issue 2 p. 301-302
Reply to “German Neurology in 1982: Society in Transition”
Heiner Fangerau MD,Michael Martin PhD,Axel Karenberg MD
doi : 10.1002/ana.26284
Volume 91, Issue 2 p. 302-302
Corrigendum: Synergistic Deoxynucleoside and Gene Therapies for Thymidine Kinase 2 Deficiency
doi : 10.1002/ana.26295
Volume 91, Issue 2 p. 303-303
