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Annals of Neurology: Volume 90, Number 5, November 2021
doi : 10.1002/ana.26247
Volume 90, Issue 5 p. C1-C1
A photomicrograph of a cultured human cell showing the subcellular distribution of the L334R variant of karyopherin-?3, which causes hereditary spastic paraplegia. Karyopherin-?3, a nuclear transport receptor that mediates trafficking of proteins between the cell cytoplasm and nucleus, normally resides almost exclusively in nuclei (labeled blue), while the disease-associated L334R variant (green) exhibits increased levels within the cytoplasm (stained red with tubulin antibodies). For more details see paper in this issue by Schob et al. (pp. 738–750).
Changing Gears – DBS For Dopaminergic Desensitization in Parkinson's Disease?
Daniel Weiss MD,Jens Volkmann MD, PhD,Alfonso Fasano MD, PhD,Andrea Kühn MD,Paul Krack MD, PhD,Günther Deuschl MD
doi : 10.1002/ana.26164
Volume 90, Issue 5 p. 699-710
In Parkinson's disease, both motor and neuropsychiatric complications unfold as a consequence of both incremental striatal dopaminergic denervation and intensifying long-term dopaminergic treatment. Together, this leads to ‘dopaminergic sensitization’ steadily increasing motor and behavioral responses to dopaminergic medication that result in the detrimental sequalae of long-term dopaminergic treatment. We review the clinical presentations of ‘dopaminergic sensitization’, including rebound off and dyskinesia in the motor domain, and neuropsychiatric fluctuations and behavioral addictions with impulse control disorders and dopamine dysregulation syndrome in the neuropsychiatric domain. We summarize state-of-the-art deep brain stimulation, and show that STN-DBS allows dopaminergic medication to be tapered, thus supporting dopaminergic desensitization. In this framework, we develop our integrated debatable viewpoint of “changing gears”, that is we suggest rethinking earlier use of subthalamic nucleus deep brain stimulation, when the first clinical signs of dopaminergic motor or neuropsychiatric complications emerge over the steadily progressive disease course. In this sense, subthalamic deep brain stimulation may help reduce longitudinal motor and neuropsychiatric symptom expression – importantly, not by neuroprotection but by supporting dopaminergic desensitization through postoperative medication reduction. Therefore, we suggest considering STN-DBS early enough before patients encounter potentially irreversible psychosocial consequences of dopaminergic complications, but importantly not before a patient shows first clinical signs of dopaminergic complications. We propose to consider neuropsychiatric dopaminergic complications as a new inclusion criterion in addition to established motor criteria, but this concept will require validation in future clinical trials. ANN NEUROL 2021;90:699–710
Single Photon Emission Computed Tomography/Positron Emission Tomography Molecular Imaging for Parkinsonism: A Fast-Developing Field
Antoine Verger MD, PhD,Stephan Grimaldi MD, MSc,Maria-Joao Ribeiro MD, PhD,Solène Frismand MD,Eric Guedj MD, PhD
doi : 10.1002/ana.26187
Volume 90, Issue 5 p. 711-719
The early differential diagnosis of Parkinson disease and atypical parkinsonism is a major challenge. The use of single photon emission computed tomography (SPECT)/positron emission tomography (PET) molecular imaging to investigate parkinsonism is a fast-developing field. Imaging biomarker research may potentially lead to more accurate disease detection, enabling earlier diagnosis and treatment. This review summarizes recent SPECT/PET advances in radiopharmaceuticals and imaging technologies/analyses that improve the diagnosis of neurodegenerative parkinsonism. We are currently witnessing a turning point in the field. Integrating molecular imaging as a diagnostic technique represents an opportunity to reassess the strategies for diagnosing neurodegenerative parkinsonism. ANN NEUROL 2021;90:711–719
ANA Investigates Therapeutic Advancements in Neuroimmunology
Rohini D. Samudralwar MD,Adeline L. Goss MD,Megan Richie MD,Jeffrey M. Gelfand MD
doi : 10.1002/ana.26222
Volume 90, Issue 5 p. 720-721
CD20+ T Cells as Pathogenic Players and Therapeutic Targets in MS
Edgar Meinl MD,Reinhard Hohlfeld MD
doi : 10.1002/ana.26232
Volume 90, Issue 5 p. 722-724
Neuropathological Variability within a Spectrum of NMDAR-Encephalitis
Tobias Zrzavy MD, PhD,Verena Endmayr MSc,Jan Bauer PhD,Stefan Macher MD,Nilufar Mossaheb MD,Carmen Schwaiger MSc,Gerda Ricken MSc,Michael Winklehner MD,Sarah Glatter MD,Markus Breu MD, PhD,Isabella Wimmer PhD,Gabor G. Kovacs MD, PhD,Daniele U. Risser MD,Nikolaus Klupp MD,Ingrid Simonitsch-Klupp MD,Thomas Roetzer MD,Paulus Rommer MD,Thomas Berger MD, MSc,Ellen Gelpi MD, PhD,Hans Lassmann MD,Francesc Graus MD, PhD,Josep Dalmau MD, PhD,Romana Höftberger MD
doi : 10.1002/ana.26223
Volume 90, Issue 5 p. 725-737
To describe the neuropathological features of N-methyl-D-aspartate receptor (NMDAR)-encephalitis in an archival autopsy cohort.
Dominant KPNA3 Mutations Cause Infantile-Onset Hereditary Spastic Paraplegia
Claudia Schob MD,Maja Hempel MD,Dana Safka Brozkova MD, PhD,Huafang Jiang,Soo Yeon Kim MD,Nurit Assia Batzir MD,Naama Orenstein MD,Tatjana Bierhals MD,Jessika Johannsen MD,Anna Uhrova Meszarosova MS,Jong-Hee Chae MD,Pavel Seeman MD, PhD,Mathias Woidy,Fang Fang MD,Christian Kubisch MD,Stefan Kindler PhD,Jonas Denecke MD
doi : 10.1002/ana.26228
Volume 90, Issue 5 p. 738-750
Hereditary spastic paraplegia (HSP) is a highly heterogeneous neurologic disorder characterized by lower-extremity spasticity. Here, we set out to determine the genetic basis of an autosomal dominant, pure, and infantile-onset form of HSP in a cohort of 8 patients with a uniform clinical presentation.
Tau-Atrophy Variability Reveals Phenotypic Heterogeneity in Alzheimer's Disease
Sandhitsu R. Das PhD,Xueying Lyu BA,Michael Tran Duong BA,Long Xie PhD,Lauren McCollum MD,Robin de Flores PhD,Michael DiCalogero BA,David J. Irwin MD,Bradford C. Dickerson MD,Ilya M. Nasrallah MD,Paul A. Yushkevich PhD,David A. Wolk MD,Alzheimer's Disease Neuroimaging Initiative
doi : 10.1002/ana.26233
Volume 90, Issue 5 p. 751-762
Tau neurofibrillary tangles (T) are the primary driver of downstream neurodegeneration (N) and subsequent cognitive impairment in Alzheimer's disease (AD). However, there is substantial variability in the T-N relationship – manifested in higher or lower atrophy than expected for level of tau in a given brain region. The goal of this study was to determine if region-based quantitation of this variability allows for identification of underlying modulatory factors, including polypathology.
Relation of Pre-Stroke Aspirin Use With Cerebral Infarct Volume and Functional Outcomes
Wi-Sun Ryu MD, PhD,Dawid Schellingerhout MD,Keun-Sik Hong MD, PhD,Sang-Wuk Jeong MD, PhD,Beom Joon Kim MD, PhD,Joon-Tae Kim MD, PhD,Kyung Bok Lee MD, PhD,Tai Hwan Park MD, PhD,Sang-Soon Park MD,Jong-Moo Park MD, PhD,Kyusik Kang MD, PhD,Yong-Jin Cho MD, PhD,Hong-Kyun Park MD, MSc,Byung-Chul Lee MD, PhD,Kyung-Ho Yu MD, PhD,Mi Sun Oh MD, PhD,Soo Joo Lee MD, PhD,Jae Guk Kim MD, MSc,Jae-Kwan Cha MD, PhD,Dae-Hyun Kim MD, PhD,Jun Lee MD, PhD,Moon-Ku Han MD, PhD,Man Seok Park MD,Kang-Ho Choi MD, PhD,Matthias Nahrendorf MD, PhD,Juneyoung Lee PhD,Hee-Joon Bae MD, PhD,Dong-Eog Kim MD, PhD
doi : 10.1002/ana.26219
Volume 90, Issue 5 p. 763-776
We investigated (1) the associations of pre-stroke aspirin use with thrombus burden, infarct volume, hemorrhagic transformation, early neurological deterioration (END), and functional outcome, and (2) whether stroke subtypes modify these associations in first-ever ischemic stroke.
Genome-Wide Association Study Identifies First Locus Associated with Susceptibility to Cerebral Venous Thrombosis
Gie Ken-Dror PhD,Ioana Cotlarciuc PhD,Ida Martinelli MD, PhD,Elvira Grandone MD, PhD,Sini Hiltunen MD,Erik Lindgren MD,Maurizio Margaglione MD,Veronique Le Cam Duchez MD, PhD,Aude Bagan Triquenot MD,Marialuisa Zedde MD,Michelangelo Mancuso MD, PhD,Ynte M. Ruigrok MD,Thomas Marjot MRCP,Brad Worrall MD, MSc,Jennifer J. Majersik MD, MS,Tiina M. Metso MD,Jukka Putaala MD, PhD,Elena Haapaniemi MD, PhD,Susanna M. Zuurbier MD, PhD,Matthijs C. Brouwer MD, PhD,Serena M. Passamonti BSc,Maria Abbattista MSc,Paolo Bucciarelli MD,Braxton D. Mitchell PhD, MPH,Steven J. Kittner MD, MPH,Robin Lemmens MD, PhD,Christina Jern MD, PhD,Emanuela Pappalardo MS,Paolo Costa MD,Marina Colombi PhD,Diana Aguiar de Sousa MD, MSc,Sofia Rodrigues MD,Patrícia Canhão MD, PhD,Aleksander Tkach MD,Rosa Santacroce MD,Giovanni Favuzzi MD,Antonio Arauz MD, MSc,Donatella Colaizzo BSc,Kostas Spengos MD, PhD,Amanda Hodge MSc,Reina Ditta MSc,Alessandro Pezzini MD,Stephanie Debette MD, PhD,Jonathan M. Coutinho MD, PhD,Vincent Thijs PhD,Katarina Jood MD,Guillaume Pare MD, MSc,Turgut Tatlisumak MD, PhD,José M. Ferro MD, PhD,Pankaj Sharma MD, PhD
doi : 10.1002/ana.26205
Volume 90, Issue 5 p. 777-788
Cerebral venous thrombosis (CVT) is an uncommon form of stroke affecting mostly young individuals. Although genetic factors are thought to play a role in this cerebrovascular condition, its genetic etiology is not well understood.
Neuronal TNF?, Not ?-Syn, Underlies PDD-Like Disease Progression in IFN?-KO Mice
Erika B. Villanueva,Emilie Tresse,Yawei Liu,João N. Duarte,Gisela Jimenez-Duran,Patrick Ejlerskov,Oliver Kretz,Desiree Loreth,Tobias Goldmann,Marco Prinz,Shohreh Issazadeh-Navikas
doi : 10.1002/ana.26209
Volume 90, Issue 5 p. 789-807
Parkinson's disease (PD) manifests in motor dysfunction, non-motor symptoms, and eventual dementia (PDD). Neuropathological hallmarks include nigrostriatal neurodegeneration, Lewy body (LB) pathology, and neuroinflammation. Alpha-synuclein (?-syn), a primary component of LBs, is implicated in PD pathogenesis, accumulating, and aggregating in both familial and sporadic PD. However, as ?-syn pathology is often comorbid with amyloid-beta (A?) plaques and phosphorylated tau (pTau) tangles in PDD, it is still unclear whether ?-syn is the primary cause of neurodegeneration in sporadic PDD. We aimed to determine how the absence of ?-syn would affect PDD manifestation.
Seizures after Ischemic Stroke: A Matched Multicenter Study
Carolina Ferreira-Atuesta MD,Nico Döhler MD,Barbara Erdélyi-Canavese MD,Ansgar Felbecker MD,Philip Siebel MD,Natalie Scherrer MD,Giulio Bicciato MD,Juliane Schweizer MD,Lucia Sinka MD,Lukas L. Imbach MSc,Mira Katan MD,Laura Abraira MD,Estevo Santamarina MD,José Álvarez-Sabín PhD,Michael Winklehner MD,Tim J. von Oertzen FRCP,Judith N. Wagner MD,Gian Luigi Gigli MD,Anna Serafini MD,Francesco Janes PhD,Giovanni Merlino PhD,Mariarosaria Valente MD,Giorgia Gregoraci MD,Julian Conrad MD,Stefan Evers PhD,Piergiorgio Lochner MD,Frauke Roell MD,Francesco Brigo MD,Carla Bentes PhD,Ana Rita Peralta MD,Teresa Pinho e Melo MD,Mark R. Keezer MDCM,John S. Duncan FRCP,Josemir W. Sander FRCP,Barbara Tettenborn MD,Matthias J. Koepp PhD,Marian Galovic MD
doi : 10.1002/ana.26212
Volume 90, Issue 5 p. 808-820
The purpose of this study was to identify risk factors for acute symptomatic seizures and post-stroke epilepsy after acute ischemic stroke and evaluate the effects of reperfusion treatment.
Thalamic Influence on Slow Wave Slope Renormalization During Sleep
Valeria Jaramillo PhD,Jasmine Jendoubi MSc,Angelina Maric PhD,Armand Mensen PhD,Natalie C. Heyse MSc,Aleksandra K. Eberhard-Moscicka PhD,Roland Wiest MD,Claudio L. A. Bassetti MD,Reto Huber PhD
doi : 10.1002/ana.26217
Volume 90, Issue 5 p. 821-833
Slow waves are thought to mediate an overall reduction in synaptic strength during sleep. The specific contribution of the thalamus to this so-called synaptic renormalization is unknown. Thalamic stroke is associated with daytime sleepiness, along with changes to sleep electroencephalography and cognition, making it a unique “experiment of nature” to assess the relationship between sleep rhythms, synaptic renormalization, and daytime functions.
Proinflammatory CD20+ T Cells are Differentially Affected by Multiple Sclerosis Therapeutics
Corinna Quendt MD,Jasmin Ochs PhD,Silke Häusser-Kinzel PhD,Darius Häusler PhD,Martin S. Weber MD
doi : 10.1002/ana.26216
Volume 90, Issue 5 p. 834-839
The frequency of CD20+ T cells was reported to be increased in several inflammatory conditions. We report that in patients with multiple sclerosis (MS), CD20+ T cells display a distinct proinflammatory phenotype with pathogenic properties. Anti-CD20 treatment virtually extinguished CD20+ T cells, which might explain its broad effectiveness. Dimethyl fumarate dampened activity of differentiated CD20+ T cells, whereas fingolimod reduced their abundance only as part of its overall T cell suppressive capacity. Natalizumab increased the frequency of CD20+ effector T cells. Widely used MS therapeutics affect this proinflammatory T cell subset with assumed pathogenic potential in a surprisingly differential manner. ANN NEUROL 2021 ANN NEUROL 2021;90:834–839
Sleep Deprivation Exacerbates Seizures and Diminishes GABAergic Tonic Inhibition
Sai Surthi Konduru MD,Yu-Zhen Pan PhD,Eli Wallace PhD,Jesse A. Pfammatter PhD,Mathew V. Jones PhD,Rama K. Maganti MD
doi : 10.1002/ana.26208
Volume 90, Issue 5 p. 840-844
Patients with epilepsy report that sleep deprivation is a common trigger for breakthrough seizures. The basic mechanism of this phenomenon is unknown. In the Kv1.1?/? mouse model of epilepsy, daily sleep deprivation indeed exacerbated seizures though these effects were lost after the third day. Sleep deprivation also accelerated mortality in ~?52% of Kv1.1?/? mice, not observed in controls. Voltage-clamp experiments on the day after recovery from sleep deprivation showed reductions in GABAergic tonic inhibition in dentate granule cells in epileptic Kv1.1?/? mice. Our results suggest that sleep deprivation is detrimental to seizures and survival, possibly due to reductions in GABAergic tonic inhibition. ANN NEUROL 2021;90:840–844
Ablating the Transporter Sodium-Dependent Dicarboxylate Transporter 3 Prevents Leukodystrophy in Canavan Disease Mice
Yan Wang PhD,Vanessa Hull MS,Sarah Sternbach BS,Brad Popovich BA,Travis Burns BS,Jennifer McDonough PhD,Fuzheng Guo PhD,David Pleasure MD
doi : 10.1002/ana.26211
Volume 90, Issue 5 p. 845-850
Canavan disease is caused by ASPA mutations that diminish brain aspartoacylase activity, and it is characterized by excessive brain storage of the aspartoacylase substrate, N-acetyl-l-aspartate (NAA), and by astroglial and intramyelinic vacuolation. Astroglia and the arachnoid mater express sodium-dependent dicarboxylate transporter (NaDC3), encoded by SLC13A3, a sodium-coupled transporter for NAA and other dicarboxylates. Constitutive Slc13a3 deletion in aspartoacylase-deficient Canavan disease mice prevents brain NAA overaccumulation, ataxia, and brain vacuolation. ANN NEUROL 2021;90:845–850
Typical Radiological Features of a Rare Lateral Ventricular Liponeurocytoma
Sisi Shen MD,Yao Tang MD,Ruiyi Yang MD,Dong Zhou MD
doi : 10.1002/ana.26207
Volume 90, Issue 5 p. 851-852
Hypoparathyroidism Associated with Vascular Centrum Semiovale Calcifications
Cassiana Trandafir MD,Dimitri Renard MD
doi : 10.1002/ana.26210
Volume 90, Issue 5 p. 853-854
Core Penumbral Mismatch: An Independent Predictor of Stroke Poorer Outcome
Basile Kerleroux MD, MSc,Grégoire Boulouis MD, PhD
doi : 10.1002/ana.26229
Volume 90, Issue 5 p. 855-855
Reply to “Core Penumbral Mismatch: An Independent Predictor of Stroke Poorer Outcome”
Pierre Seners MD, PhD,Jean-Marc Olivot MD, PhD
doi : 10.1002/ana.26224
Volume 90, Issue 5 p. 855-856
Guillain-Barré Syndrome in an Australian State Using Both mRNA and Adenovirus-Vector SARS-CoV-2 Vaccines
Joshua Osowicki PhD,Hannah Morgan MPH,Adele Harris RN,Nigel W. Crawford PhD,Jim P. Buttery PhD,Lynette Kiers MD
doi : 10.1002/ana.26218
Volume 90, Issue 5 p. 856-858
