LIVIVO - Search results -

Search results

Result 1 - 9 of total 9

Search options

Article: Neuromyelitis Optica Spectrum Disorder Resembling Wernicke's Encephalopathy: A Case Report and Review of the Literature.

Lynch, Sloan / Saez Calveras, Nil / Amin, Anik

2024 Volume 14, Issue 2, Page(s) 213–217

Abstract: We describe a case of Neuromyelitis Optica Spectrum Disorder (NMOSD) mimicking Wernicke's Encephalopathy (WE) to highlight an atypical presentation of NMOSD. A 39-year-old female presented with subacute encephalopathy and progressive ophthalmoplegia. Her ...

Abstract	We describe a case of Neuromyelitis Optica Spectrum Disorder (NMOSD) mimicking Wernicke's Encephalopathy (WE) to highlight an atypical presentation of NMOSD. A 39-year-old female presented with subacute encephalopathy and progressive ophthalmoplegia. Her MRI revealed T2 hyperintensities involving the mammillary bodies, periaqueductal grey matter, medial thalami, third ventricle, and area postrema. Whole blood thiamine levels were elevated and she did not improve with IV thiamine. CSF was notable for lymphocytic pleocytosis and elevated protein. She tested positive for serum Aquaporin-4 (AQP4) antibody. Subsequent imaging revealed multilevel lesions in the cervical and thoracic spinal cord. Her CSF GFAP antibody also came back positive. She steadily and significantly improved after high-dose IV steroids and plasmapheresis. She later started on chronic rituximab therapy. This represents a unique case of NMOSD presenting with the classical clinical and imaging features of WE, as opposed to the typical presenting symptoms of NMOSD. As such, demyelinating disorders should be considered when there is concern for diencephalic and midline pathologies, particularly without classic WE risk factors. Conversely, clinicians should be aware of secondary nutritional complications arising from severe area postrema syndrome.
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Case Reports
ZDB-ID	2629083-2
ISSN	1941-8752 ; 1941-8744
ISSN (online)	1941-8752
ISSN	1941-8744
DOI	10.1177/19418744241228004
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: The role of the complement system in Multiple Sclerosis: A review.

Saez-Calveras, Nil / Stuve, Olaf

Frontiers in immunology

2022 Volume 13, Page(s) 970486

Abstract: The complement system has been involved in the pathogenesis of multiple neuroinflammatory and neurodegenerative conditions. In this review, we evaluated the possible role of complement activation in multiple sclerosis (MS) with a focus in progressive MS, ...

Abstract	The complement system has been involved in the pathogenesis of multiple neuroinflammatory and neurodegenerative conditions. In this review, we evaluated the possible role of complement activation in multiple sclerosis (MS) with a focus in progressive MS, where the disease pathogenesis remains to be fully elucidated and treatment options are limited. The evidence for the involvement of the complement system in the white matter plaques and gray matter lesions of MS stems from immunohistochemical analysis of post-mortem MS brains,
MeSH term(s)	Animals ; Complement System Proteins ; Encephalomyelitis, Autoimmune, Experimental ; Epstein-Barr Virus Infections ; Humans ; Multiple Sclerosis
Chemical Substances	Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.970486
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Limb myorhythmia treated with chemodenervation: a case report.

Saez-Calveras, Nil / Bryarly, Meredith / Salinas, Meagen

Therapeutic advances in neurological disorders

2023 Volume 16, Page(s) 17562864221150317

Abstract: We describe a case of limb myorhythmia successfully palliated with botulinum toxin injections. The patient is a 30-year-old male evaluated for abnormal movements of the left lower foot that began after an ankle injury for which the patient underwent ... ...

Abstract	We describe a case of limb myorhythmia successfully palliated with botulinum toxin injections. The patient is a 30-year-old male evaluated for abnormal movements of the left lower foot that began after an ankle injury for which the patient underwent Achilles tendon scar tissue debridement without improvement. On examination, he had near-constant involuntary, slow, rhythmic flexion/extension tremor of toes 2-4 that was diminished during active movement. Needle electromyography (EMG) revealed a rhythmic, 2-3 Hz tremor isolated to the flexor digitorum brevis. After failure of medical management with muscle relaxants, gabapentin, and levodopa trials, the patient underwent two EMG-guided chemodenervation procedures with incobotulinum toxin A injections of the left flexor digitorum brevis. At 3-month follow-up, he had achieved a sustained 50% reduction in the intensity of the movements and improved quality of life. Myorhythmia is a rare condition characterized by a repetitive, rhythmic, slow frequency (1-4 Hz) movement affecting the cranial and limb muscles. The most common causes include stroke, demyelinating disorders, drug or toxin intake, trauma, and infections. The management of this condition is very limited with pharmacologic agents such as anticholinergics, antispasmodics, anticonvulsants, or dopaminergic agents showing limited efficacy. The use of botulinum toxin chemodenervation aided by EMG muscle targeting can be a useful therapeutic intervention in cases of medication-refractory regionally distributed myorhythmia involving accessible muscles.
Language	English
Publishing date	2023-03-24
Publishing country	England
Document type	Case Reports
ZDB-ID	2442245-9
ISSN	1756-2864 ; 1756-2856
ISSN (online)	1756-2864
ISSN	1756-2856
DOI	10.1177/17562864221150317
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Episodic stuttering as the presenting manifestation of acute ischemic stroke: A case report and systematic literature review.

Saez-Calveras, Nil / Tran, Nguyen / Tran, Conny / Upadhyaya, Parth

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association

2023 Volume 32, Issue 9, Page(s) 107271

Abstract: Background: Acquired episodic stuttering in adulthood represents a rare condition, which has been infrequently described in the literature.: Case presentation: We describe the case of a 62-year-old male who presented to the emergency room with three ... ...

Abstract	Background: Acquired episodic stuttering in adulthood represents a rare condition, which has been infrequently described in the literature. Case presentation: We describe the case of a 62-year-old male who presented to the emergency room with three episodes of new-onset brief isolated stuttering with no other speech impairment or associated focal neurologic deficits. His brain magnetic resonance imaging was notable for the presence of a small acute ischemic stroke involving the left precuneus cortex. Systematic literature review: We performed a systematic literature review to evaluate the association between stroke and acquired neurogenic stuttering. The evidence published to this date suggests that the underlying pathophysiology of acquired stutter does not localize to an isolated or focal region. The development of stuttering secondary to strokes may be the result of a disruption at any level in a cortico-striato-cortical integrative pathway mediating speech execution. Conclusion: Here we aimed to emphasize the importance of carefully evaluating new-onset recurrent episodic stuttering to rule out an underlying stroke or another neurogenic etiology. We provide a comprehensive review of acquired stuttering, its differential diagnosis, and its evaluation.
MeSH term(s)	Male ; Humans ; Middle Aged ; Stuttering/diagnosis ; Stuttering/etiology ; Ischemic Stroke/diagnosis ; Ischemic Stroke/diagnostic imaging ; Brain ; Speech ; Stroke/diagnosis ; Stroke/diagnostic imaging
Language	English
Publishing date	2023-07-27
Publishing country	United States
Document type	Systematic Review ; Case Reports
ZDB-ID	1131675-5
ISSN	1532-8511 ; 1052-3057
ISSN (online)	1532-8511
ISSN	1052-3057
DOI	10.1016/j.jstrokecerebrovasdis.2023.107271
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3519: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: The validity of animal models to explore the pathogenic role of the complement system in multiple sclerosis: A review.

Saez-Calveras, Nil / Brewster, Amy L / Stuve, Olaf

Frontiers in molecular neuroscience

2022 Volume 15, Page(s) 1017484

Abstract: Animal models of multiple sclerosis (MS) have been extensively used to characterize the disease mechanisms in MS, as well as to identify potential pharmacologic targets for this condition. In recent years, the immune complement system has gained ... ...

Abstract	Animal models of multiple sclerosis (MS) have been extensively used to characterize the disease mechanisms in MS, as well as to identify potential pharmacologic targets for this condition. In recent years, the immune complement system has gained increased attention as an important effector in the pathogenesis of MS. Evidence from histological, serum, and CSF studies of patients supports an involvement of complement in both relapsing-remitting and progressive MS. In this review, we discuss the history and advances made on the use of MS animal models to profile the effects of the complement system in this condition. The first studies that explored the complement system in the context of MS used cobra venom factor (CVF) as a complement depleting agent in experimental autoimmune encephalomyelitis (EAE) Lewis rats. Since then, multiple mice and rat models of MS have revealed a role of C3 and the alternative complement cascade in the opsonization and phagocytosis of myelin by microglia and myeloid cells. Studies using viral vectors, genetic knockouts and pharmacologic complement inhibitors have also shown an effect of complement in synaptic loss. Antibody-mediated EAE models have revealed an involvement of the C1 complex and the classical complement as an effector of the humoral response in this disease. C1q itself may also be involved in modulating microglia activation and oligodendrocyte differentiation in these animals. In addition, animal and
Language	English
Publishing date	2022-10-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2022.1017484
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Blood Markers in Relation to a History of Traumatic Brain Injury Across Stages of Cognitive Impairment in a Diverse Cohort.

LoBue, Christian / Stopschinski, Barbara E / Saez Calveras, Nil / Douglas, Peter M / Huebinger, Ryan / Cullum, C Munro / Hart, John / Gonzales, Mitzi M

Journal of Alzheimer's disease : JAD

2023 Volume 97, Issue 1, Page(s) 345–358

Abstract: Background: Traumatic brain injury (TBI) has been linked to multiple pathophysiological processes that could increase risk for Alzheimer's disease and related dementias (ADRD). However, the impact of prior TBI on blood biomarkers for ADRD remains ... ...

Abstract	Background: Traumatic brain injury (TBI) has been linked to multiple pathophysiological processes that could increase risk for Alzheimer's disease and related dementias (ADRD). However, the impact of prior TBI on blood biomarkers for ADRD remains unknown. Objective: Using cross-sectional data, we assessed whether a history of TBI influences serum biomarkers in a diverse cohort (approximately 50% Hispanic) with normal cognition, mild cognitive impairment, or dementia. Methods: Levels of glial fibrillary acidic protein (GFAP), neurofilament light (NFL), total tau (T-tau), and ubiquitin carboxy-terminal hydrolase-L1 (UCHL1) were measured for participants across the cognitive spectrum. Participants were categorized based on presence and absence of a history of TBI with loss of consciousness, and study samples were derived through case-control matching. Multivariable general linear models compared concentrations of biomarkers in relation to a history of TBI and smoothing splines modelled biomarkers non-linearly in the cognitively impaired groups as a function of time since symptom onset. Results: Each biomarker was higher across stages of cognitive impairment, characterized by clinical diagnosis and Mini-Mental State Examination performance, but these associations were not influenced by a history of TBI. However, modelling biomarkers in relation to duration of cognitive symptoms for ADRD showed differences by history of TBI, with only GFAP and UCHL1 being elevated. Conclusions: Serum GFAP, NFL, T-tau, and UCHL1 were higher across stages of cognitive impairment in this diverse clinical cohort, regardless of TBI history, though longitudinal investigation of the timing, order, and trajectory of the biomarkers in relation to prior TBI is warranted.
MeSH term(s)	Humans ; Cross-Sectional Studies ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/diagnosis ; Alzheimer Disease ; Biomarkers ; Cognitive Dysfunction/diagnosis ; Glial Fibrillary Acidic Protein
Chemical Substances	Biomarkers ; Glial Fibrillary Acidic Protein
Language	English
Publishing date	2023-12-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-231027
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6084: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Microglia as a cellular target of diclofenac therapy in Alzheimer's disease.

Stopschinski, Barbara E / Weideman, Rick A / McMahan, Danni / Jacob, David A / Little, Bertis B / Chiang, Hsueh-Sheng / Saez Calveras, Nil / Stuve, Olaf

Therapeutic advances in neurological disorders

2023 Volume 16, Page(s) 17562864231156674

Abstract: Alzheimer's disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. Research of the past decades has ... ...

Abstract	Alzheimer's disease (AD) is an untreatable cause of dementia, and new therapeutic approaches are urgently needed. AD pathology is defined by extracellular amyloid plaques and intracellular neurofibrillary tangles. Research of the past decades has suggested that neuroinflammation plays a critical role in the pathophysiology of AD. This has led to the idea that anti-inflammatory treatments might be beneficial. Early studies investigated non-steroidal anti-inflammatory drugs (NSAIDS) such as indomethacin, celecoxib, ibuprofen, and naproxen, which had no benefit. More recently, protective effects of diclofenac and NSAIDs in the fenamate group have been reported. Diclofenac decreased the frequency of AD significantly compared to other NSAIDs in a large retrospective cohort study. Diclofenac and fenamates share similar chemical structures, and evidence from cell and mouse models suggests that they inhibit the release of pro-inflammatory mediators from microglia with leads to the reduction of AD pathology. Here, we review the potential role of diclofenac and NSAIDs in the fenamate group for targeting AD pathology with a focus on its potential effects on microglia.
Language	English
Publishing date	2023-02-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2442245-9
ISSN	1756-2864 ; 1756-2856
ISSN (online)	1756-2864
ISSN	1756-2856
DOI	10.1177/17562864231156674
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: [

Marquié, Marta / Agüero, Cinthya / Amaral, Ana C / Villarejo-Galende, Alberto / Ramanan, Prianca / Chong, Michael Siao Tick / Sáez-Calveras, Nil / Bennett, Rachel E / Verwer, Eline E / Kim, Sally Ji Who / Dhaynaut, Maeva / Alvarez, Victor E / Johnson, Keith A / McKee, Ann C / Frosch, Matthew P / Gómez-Isla, Teresa

Acta neuropathologica communications

2019 Volume 7, Issue 1, Page(s) 164

Abstract: Introduction: Chronic traumatic encephalopathy (CTE) is a tauopathy associated to repetitive head trauma. There are no validated in vivo biomarkers of CTE and a definite diagnosis can only be made at autopsy. Recent studies have shown that positron ... ...

Abstract	Introduction: Chronic traumatic encephalopathy (CTE) is a tauopathy associated to repetitive head trauma. There are no validated in vivo biomarkers of CTE and a definite diagnosis can only be made at autopsy. Recent studies have shown that positron emission tomography (PET) tracer AV-1451 (Flortaucipir) exhibits high binding affinity for paired helical filament (PHF)-tau aggregates in Alzheimer (AD) brains but relatively low affinity for tau lesions in other tauopathies like temporal lobal degeneration (FTLD)-tau, progressive supranuclear palsy (PSP) or corticobasal degeneration (CBD). Little is known, however, about the binding profile of this ligand to the tau-containing lesions of CTE. Objective: To study the binding properties of [ Methods: We performed [ Results: Despite the presence of abundant tau aggregates in multiple regions in all CTE brains, only faint or no [ Conclusion: AV-1451 may have limited utility for in vivo selective and reliable detection of tau aggregates in CTE. The existence of disease-specific tau conformations may likely explain the differential binding affinity of this tracer for tau lesions in different tauopathies.
MeSH term(s)	Aged ; Aged, 80 and over ; Brain/metabolism ; Brain/pathology ; Carbolines ; Chronic Traumatic Encephalopathy/complications ; Chronic Traumatic Encephalopathy/metabolism ; Chronic Traumatic Encephalopathy/pathology ; Female ; Humans ; Male ; Middle Aged ; Positron-Emission Tomography ; Tauopathies/complications ; Tauopathies/metabolism ; Tauopathies/pathology ; tau Proteins/analysis ; tau Proteins/metabolism
Chemical Substances	Carbolines ; MAPT protein, human ; tau Proteins ; 7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole (J09QS3Z3WB)
Language	English
Publishing date	2019-10-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-019-0808-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: [F-18]-AV-1451 binding correlates with postmortem neurofibrillary tangle Braak staging.

Marquié, Marta / Siao Tick Chong, Michael / Antón-Fernández, Alejandro / Verwer, Eline E / Sáez-Calveras, Nil / Meltzer, Avery C / Ramanan, Prianca / Amaral, Ana C / Gonzalez, Jose / Normandin, Marc D / Frosch, Matthew P / Gómez-Isla, Teresa

Acta neuropathologica

2017 Volume 134, Issue 4, Page(s) 619–628

Abstract: F-18]-AV-1451, a PET tracer specifically developed to detect brain neurofibrillary tau pathology, has the potential to facilitate accurate diagnosis of Alzheimer's disease (AD), staging of brain tau burden and monitoring disease progression. Recent PET ... ...

Abstract	[F-18]-AV-1451, a PET tracer specifically developed to detect brain neurofibrillary tau pathology, has the potential to facilitate accurate diagnosis of Alzheimer's disease (AD), staging of brain tau burden and monitoring disease progression. Recent PET studies show that patients with mild cognitive impairment and AD dementia exhibit significantly higher in vivo [F-18]-AV-1451 retention than cognitively normal controls. Importantly, PET patterns of [F-18]-AV-1451 correlate well with disease severity and seem to match the predicted topographic Braak staging of neurofibrillary tangles (NFTs) in AD, although this awaits confirmation. We studied the correlation of autoradiographic binding patterns of [F-18]-AV-1451 and the stereotypical spatiotemporal pattern of progression of NFTs using legacy postmortem brain samples representing different Braak NFT stages (I-VI). We performed [F-18]-AV-1451 phosphor-screen autoradiography and quantitative tau measurements (stereologically based NFT counts and biochemical analysis of tau pathology) in three brain regions (entorhinal cortex, superior temporal sulcus and visual cortex) in a total of 22 cases: low Braak (I-II, n = 6), intermediate Braak (III-IV, n = 7) and high Braak (V-VI, n = 9). Strong and selective [F-18]-AV-1451 binding was detected in all tangle-containing regions matching precisely the observed pattern of PHF-tau immunostaining across the different Braak stages. As expected, no signal was detected in the white matter or other non-tangle containing regions. Quantification of [F-18]-AV-1451 binding was very significantly correlated with the number of NFTs present in each brain region and with the total tau and phospho-tau content as reported by Western blot and ELISA. [F-18]-AV-1451 is a promising biomarker for in vivo quantification of brain tau burden in AD. Neuroimaging-pathologic studies conducted on postmortem material from individuals imaged while alive are now needed to confirm these observations.
MeSH term(s)	Aged ; Aged, 80 and over ; Autoradiography ; Blotting, Western ; Brain/diagnostic imaging ; Brain/metabolism ; Brain/pathology ; Carbolines ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neurofibrillary Tangles/metabolism ; Neurofibrillary Tangles/pathology ; Phosphorylation ; Plaque, Amyloid/metabolism ; Plaque, Amyloid/pathology ; Radiopharmaceuticals ; Severity of Illness Index ; tau Proteins/metabolism
Chemical Substances	Carbolines ; MAPT protein, human ; Radiopharmaceuticals ; tau Proteins ; 7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole (J09QS3Z3WB)
Language	English
Publishing date	2017-06-13
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-017-1740-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ui II Zs.188: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito