Results 181 to 190 of about 1,670,297 (269)

Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Aquaporin‐4‐IgG seropositive neuromyelitis optica spectrum disorder (AQP4+ NMOSD), myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD), and multiple sclerosis (MS) are pathophysiologically distinct neuroinflammatory disorders. Complement activation is a major mechanism of injury in AQP4+ NMOSD, whereas its role in
Angeliki G. Filippatou   +23 more
wiley   +1 more source

Dysregulated Cholesterol Metabolism, Chronic Inflammation, and Disability in Severe Progressive Multiple Sclerosis

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Background Dysregulated lipid metabolism, which can affect remyelination and neural repair, has not been extensively investigated in progressive multiple sclerosis (PMS). The goal was to examine whether dysregulated cholesterol metabolism was associated with disability in PMS. Methods The study sample comprised 53 Severe PMS patients (Expanded
Taylor R. Wicks   +8 more
wiley   +1 more source

Complementing Engel Classification: Postoperative Scalp EEG as an Objective Indicator in SEEG‐Guided Radiofrequency Thermocoagulation—A Seizure‐Onset Pattern‐Based Stratified Analysis—

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Background Stereoelectroencephalography‐guided radiofrequency thermocoagulation (SEEG‐RFTC) is a minimally invasive therapy for drug‐resistant focal epilepsy. However, the relationship between specific seizure‐onset patterns (SOPs), particularly low‐voltage fast activity (LVFA), and postoperative scalp EEG normalization remains inadequately ...
Yi‐qing Yang   +6 more
wiley   +1 more source

Juvenile Huntington Disease With Cerebellar‐Predominant Atrophy Identified by Genome Sequencing

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Juvenile Huntington disease accounts for a small fraction of Huntington disease cases and is driven by the largest trinucleotide repeat expansions. We describe a 6‐year‐old boy with progressive global regression, generalized dystonia, and epilepsy, in whom serial imaging showed striking cerebellar‐predominant atrophy with an initially normal ...
Enrique Gonzalez Saez‐Diez   +5 more
wiley   +1 more source

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