scholarly journals Association of Developmental Venous Anomalies with Demyelinating Lesions in Patients with Multiple Sclerosis

2017 ◽  
Vol 39 (1) ◽  
pp. 97-101 ◽  
Author(s):  
D.M. Rogers ◽  
M.E. Peckham ◽  
L.M. Shah ◽  
R.H. Wiggins
Keyword(s):  
Multiple Sclerosis ◽  
Venous Anomalies ◽  
Demyelinating Lesions ◽  
Developmental Venous Anomalies

827 Central Sleep Apnea in a patient with Multiple Sclerosis

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A322-A323
Author(s):  
Rahul Dasgupta ◽  
Sonja Schütz ◽  
Tiffany Braley
Keyword(s):  
Multiple Sclerosis ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Disordered Breathing ◽  
Central Sleep Apnea ◽  
Progressive Multiple Sclerosis ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Demyelinating Lesions ◽  
The Brain

Abstract Introduction Sleep-disordered breathing is common in persons with multiple sclerosis (PwMS), and may contribute to debilitating fatigue and other chronic MS symptoms. The majority of research to date on SDB in MS has focused on the prevalence and consequences of obstructive sleep apnea; however, PwMS may also be at increased risk for central sleep apnea (CSA), and the utility of methods to assess CSA in PwMS warrant further exploration. We present a patient with secondary progressive multiple sclerosis who was found to have severe central sleep apnea on WatchPAT testing. Report of case(s) A 61 year-old female with a past medical history of secondary progressive multiple sclerosis presented with complaints of fragmented sleep. MRI of the brain, cervical spine, and thoracic spine showed numerous demyelinating lesions in the brain, brainstem, cervical, and thoracic spinal cord. Upon presentation, the patient noted snoring, witnessed apneas, and daytime sleepiness. WatchPAT demonstrated severe sleep apnea, with a pAHI of 63.3, and a minimum oxygen saturation of 90%. The majority of the scored events were non-obstructive in nature (73.1% of all scored events), and occurred intermittently in a periodic fashion. Conclusion The differential diagnosis of fatigue in PwMS should include sleep-disordered breathing, including both obstructive and central forms of sleep apnea. Demyelinating lesions in the brainstem (which may contribute to impairment of motor and sensory networks that control airway patency and respiratory drive), and progressive forms of MS, have been linked to both OSA and CSA. The present data illustrate this relationship in a person with progressive MS, and offer support for the WatchPAT as a cost-effective means to evaluate for both OSA and CSA in PwMS, while reducing patient burden. PwMS may be at increased risk for CSA. Careful clinical consideration should be given to ordering appropriate sleep testing to differentiate central from obstructive sleep apnea in PwMS, particularly for patients with demyelinating lesions in the brainstem. Support (if any) 1. Braley TJ, Segal BM, Chervin RD. Obstructive sleep apnea and fatigue in patients with multiple sclerosis. J Clin Sleep Med. 2014 Feb 15;10(2):155–62. doi: 10.5664/jcsm.3442. PMID: 24532998; PMCID: PMC3899317.

scholarly journals Microglial Pruning: Relevance for Synaptic Dysfunction in Multiple Sclerosis and Related Experimental Models

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 686
Author(s):  
Maria Concetta Geloso ◽  
Nadia D’Ambrosi
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Death ◽  
Environmental Changes ◽  
Experimental Models ◽  
Synaptic Dysfunction ◽  
Synapse Elimination ◽  
Neurodegenerative Process ◽  
Immune Mediated ◽  
Wide Range ◽  
Demyelinating Lesions

Microglia, besides being able to react rapidly to a wide range of environmental changes, are also involved in shaping neuronal wiring. Indeed, they actively participate in the modulation of neuronal function by regulating the elimination (or “pruning”) of weaker synapses in both physiologic and pathologic processes. Mounting evidence supports their crucial role in early synaptic loss, which is emerging as a hallmark of several neurodegenerative diseases, including multiple sclerosis (MS) and its preclinical models. MS is an inflammatory, immune-mediated pathology of the white matter in which demyelinating lesions may cause secondary neuronal death. Nevertheless, primitive grey matter (GM) damage is emerging as an important contributor to patients’ long-term disability, since it has been associated with early and progressive cognitive decline (CD), which seriously worsens the quality of life of MS patients. Widespread synapse loss even in the absence of demyelination, axon degeneration and neuronal death has been demonstrated in different GM structures, thus raising the possibility that synaptic dysfunction could be an early and possibly independent event in the neurodegenerative process associated with MS. This review provides an overview of microglial-dependent synapse elimination in the neuroinflammatory process that underlies MS and its experimental models.

Metabolic Changes of Brain Developmental Venous Anomalies on 18F-FDG-PET

2019 ◽  
Vol 26 (4) ◽  
pp. 443-449 ◽  
Author(s):  
Jillian W. Lazor ◽  
J. Eric Schmitt ◽  
Laurie A. Loevner ◽  
S. Ali Nabavizadeh
Keyword(s):  
Fdg Pet ◽  
Metabolic Changes ◽  
Venous Anomalies ◽  
Developmental Venous Anomalies ◽  
18F Fdg

Developmental venous anomalies with arterial supply

2008 ◽  
Vol 108 (6) ◽  
pp. 1139-1141 ◽  
Author(s):  
Stacey Quintero Wolfe ◽  
Roberto C. Heros
Keyword(s):  
Arterial Supply ◽  
Venous Anomalies ◽  
Developmental Venous Anomalies

Remyelination of Demyelinated CNS Axons by Transplanted Human Schwann Cells: The Deleterious Effect of Contaminating Fibroblasts

2001 ◽  
Vol 10 (3) ◽  
pp. 305-315 ◽  
Author(s):  
C. M. H. Brierley ◽  
A. J. Crang ◽  
Y. Iwashita ◽  
J. M. Gilson ◽  
N. J. Scolding ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Axonal Degeneration ◽  
Autologous Transplantation ◽  
Growth Factor Receptor ◽  
Adult Rats ◽  
Demyelinating Lesions ◽  
Cell Implantation

Areas of demyelination can be remyelinated by transplanting myelin-forming cells. Schwann cells are the naturally remyelinating cells of the peripheral nervous system and have a number of features that may make them attractive for cell implantation therapies in multiple sclerosis, in which spontaneous but limited Schwann cell remyelination has been well documented. Schwann cells can be expanded in vitro, potentially affording the opportunity of autologous transplantation; and they might also be spared the demyelinating process in multiple sclerosis. Although rat, cat, and monkey Schwann cells have been transplanted into rodent demyelinating lesions, the behavior of transplanted human Schwann cells has not been evaluated. In this study we examined the consequences of injecting human Schwann cells into areas of acute demyelination in the spinal cords of adult rats. We found that transplants containing significant fibroblast contamination resulted in deposition of large amounts of collagen and extensive axonal degeneration. However, Schwann cell preparations that had been purified by positive immunoselection using antibodies to human low-affinity nerve growth factor receptor containing less than 10% fibroblasts were associated with remyelination. This result indicates that fibroblast contamination of human Schwann cells represents a greater problem than would have been appreciated from previous studies.

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