scholarly journals Impact of Astrocyte Depletion upon Inflammation and Demyelination in a Murine Animal Model of Multiple Sclerosis

2019 ◽  
Vol 20 (16) ◽  
pp. 3922 ◽  
Author(s):  
Allnoch ◽  
Baumgärtner ◽  
Hansmann
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Calcium Binding ◽  
Performance Test ◽  
Intraperitoneal Administration ◽  
Clinical Signs ◽  
Aquaporin 4 ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
The Impact

Astrocytes play a key role in demyelinating diseases, like multiple sclerosis (MS), although many of their functions remain unknown. The aim of this study was to investigate the impact of astrocyte depletion upon de- and remyelination, inflammation, axonal damage, and virus distribution in Theiler`s murine encephalomyelitis (TME). Groups of two to six glial fibrillary acidic protein (GFAP)-thymidine-kinase transgenic SJL mice and SJL wildtype mice were infected with TME virus (TMEV) or mock (vehicle only). Astrocyte depletion was induced by the intraperitoneal administration of ganciclovir during the early and late phase of TME. The animals were clinically investigated while using a scoring system and a rotarod performance test. Necropsies were performed at 46 and 77 days post infection. Cervical and thoracic spinal cord segments were investigated using hematoxylin and eosin (H&E), luxol fast blue-cresyl violet (LFB), immunohistochemistry targeting Amigo2, aquaporin 4, CD3, CD34, GFAP, ionized calcium-binding adapter molecule 1 (Iba1), myelin basic protein (MBP), non-phosphorylated neurofilaments (np-NF), periaxin, S100A10, TMEV, and immunoelectron microscopy. The astrocyte depleted mice showed a deterioration of clinical signs, a downregulation and disorganization of aquaporin 4 in perivascular astrocytes accompanied by vascular leakage. Furthermore, astrocyte depleted mice showed reduced inflammation and lower numbers of TMEV positive cells in the spinal cord. The present study indicates that astrocyte depletion in virus triggered CNS diseases contributes to a deterioration of clinical signs that are mediated by a dysfunction of perivascular astrocytes.

scholarly journals Syringomyelia in demyelinating disease of the central nervous system: Report of two cases

2011 ◽  
Vol 139 (9-10) ◽  
pp. 657-660 ◽  
Author(s):  
Dejan Savic ◽  
Slobodan Vojinovic ◽  
Mirjana Spasic ◽  
Zoran Peric ◽  
Stevo Lukic
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Magnetic Resonance ◽  
Demyelinating Disease ◽  
Clinical Signs ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
The Central Nervous System

Introduction. Syringomyelia is a cavitary extension inside the spinal cord which can be either symptomatic or congenitally-idiopathic. Syringomyelia during the course of the disease in patients presenting with clinically definite multiple sclerosis was described earlier. Syringomyelia in patients presenting with a clinically isolated syndrome suggestive of multiple sclerosis is unusual. Case Outline. We present two patients presenting with demy-elinating disease of the central nervous system with syringomyelia in the cervical and thoracic spinal cord. We did not find classical clinical signs of syringomyelia in our patients, but we disclosed syringomyelia incidentally during magnetic resonance exploration. Magnetic resonance exploration using the gadolinium contrast revealed the signs of active demyelinating lesions in the spinal cord in one patient but not in the other. Conclusion. Syringomyelia in demyelinating disease of the central nervous system opens the question whether it is a coincidental finding or a part of clinical features of the disease. Differentiation of the significance of syringomyelia finding in these patients plays a role in the choice of treatment concept in such patients.

scholarly journals Association Between Thoracic Spinal Cord Gray Matter Atrophy and Disability in Multiple Sclerosis

2015 ◽  
Vol 72 (8) ◽  
pp. 897 ◽  
Author(s):  
Regina Schlaeger ◽  
Nico Papinutto ◽  
Alyssa H. Zhu ◽  
Iryna V. Lobach ◽  
Carolyn J. Bevan ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Gray Matter ◽  
Thoracic Spinal Cord ◽  
Gray Matter Atrophy ◽  
Thoracic Spinal

scholarly journals Intermittent Atrioventricular Block following Fingolimod Initiation

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
E. Gialafos ◽  
S. Gerakoulis ◽  
A. Grigoriou ◽  
V. Haina ◽  
C. Kilidireas ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Atrioventricular Block ◽  
Frequency Domain Analysis ◽  
Thoracic Spinal Cord ◽  
Sympathetic Function ◽  
Thoracic Spinal ◽  
Demyelinating Lesions ◽  
Cardiac Sympathetic Function ◽  
Upper Thoracic

A 47-year-old female patient with multiple sclerosis (MS) developed symptomatic intermittent 2nd degree atrioventricular block (AVB) of five-hour duration, five hours after the first two doses of fingolimod, that resolved completely. Frequency domain analysis of heart rate variability (HRV) revealed increased parasympathetic activity and decreased sympathetic tone, while modified Ewing tests were suggestive of impaired cardiac sympathetic function. We hypothesize that expression of this particular arrhythmia might be related to autonomic nervous system (ANS) dysfunction due to demyelinating lesions in the upper thoracic spinal cord, possibly augmented by the parasympathetic effect of the drug.

What do we currently know about thoracic spinal cord injury recovery and outcomes? A systematic review

2012 ◽  
Vol 17 (Suppl1) ◽  
pp. 52-64 ◽  
Author(s):  
Richard J. Bransford ◽  
Jens R. Chapman ◽  
Andrea C. Skelly ◽  
Ellen M. VanAlstyne
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injuries ◽  
Poor Quality ◽  
Pulmonary Complications ◽  
Level Of Evidence ◽  
Thoracic Spinal Cord ◽  
Strength Of Evidence ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
The Impact

Object The purpose of this paper was to systematically review and critically appraise the evidence for whether there are differences in outcomes or recovery after thoracic spinal cord injuries (SCIs) based on the spinal level, the timing of intervention, or cause of SCI. Methods Systematic searches were conducted using PubMed/MEDLINE through January 5, 2012. From 486 articles identified, 10 included data on the population of interest. Included studies were assigned a level of evidence (LOE) rating based on study quality, and an overall strength of evidence was assessed. To estimate the effect of injury level on patient outcomes, the relative risk and risk difference were calculated when data were available. Results From 486 citations identified, 3 registry studies and 7 retrospective cohort studies met the inclusion criteria. All were rated as being of poor quality (LOE III). Limited literature exists on the epidemiology of traumatic and nontraumatic SCI. Few studies evaluated outcomes based on SCI level within the thoracic spine. Pulmonary complications and thromboembolic events were less common in persons with lower thoracic SCI (T7–12) than in those with higher thoracic SCI (T1–6) in 2 large studies, but no differences were found in functional outcomes in 4 smaller studies. Patients undergoing earlier surgery (< 72 hours) may have fewer ventilator, ICU, and hospital days than those undergoing later surgery. One small study of SCI during repair of aortic aneurysm compared with traumatic SCI reported similar outcomes for both groups. There are substantial deficiencies in the scientific literature on thoracic SCI in regard to assessment, outcomes ratings, and effectiveness of therapy. Conclusions The overall strength of evidence for all outcomes reported is low. Definitive conclusions should not be drawn regarding the prognosis for outcome and recovery after thoracic SCI. From a physiological standpoint, additional methodologically rigorous studies that take into consideration various levels of injury in more anatomically and physiologically relevant form are needed. Use of validated, comprehensive outcomes tools are important to improve our understanding of the impact of thoracic SCI and aid in examining factors in recovery from thoracic SCI.

scholarly journals Thoracic spinal cord lesions are influenced by the degree of cervical spine involvement in multiple sclerosis

Spinal Cord ◽  
2015 ◽  
Vol 53 (7) ◽  
pp. 520-525 ◽  
Author(s):  
L H Hua ◽  
S L Donlon ◽  
M J Sobhanian ◽  
S M Portner ◽  
D T Okuda
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Cervical Spine ◽  
Spinal Cord Lesions ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

scholarly journals The Pathology of Wobbly Hedgehog Syndrome

2018 ◽  
Vol 55 (5) ◽  
pp. 711-718 ◽  
Author(s):  
Josué Díaz-Delgado ◽  
Derick B. Whitley ◽  
Ralph W. Storts ◽  
Jill J. Heatley ◽  
Sharman Hoppes ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Axonal Degeneration ◽  
Corpus Striatum ◽  
Clinical Signs ◽  
Central Nervous System Involvement ◽  
Internal Capsule ◽  
Neurologic Disease ◽  
Status Spongiosus ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal

Wobbly hedgehog syndrome (WHS) is a leading cause of neurologic disease in African pygmy hedgehogs (APHs; Atelerix albiventris). This study describes the signalment, clinical signs, gross, microscopic, and ultrastructural lesions of WHS in a cohort of 12 pet APHs. Microscopically, lesions consisted of status spongiosus of the white matter, typically bilateral and symmetrical, with myelin degeneration and loss that was accompanied by neuronal/axonal degeneration plus reactive microgliosis and mild, focal astrocytosis and astrogliosis. Lesions were most severe in the cerebellum and medulla oblongata, as well as cervical and thoracic spinal cord. Less affected areas were the corona radiata, corpus callosum, corpus striatum, internal capsule, and the mesencephalon. Ultrastructurally, the lesions consisted of splitting of the myelin sheath at the intraperiod line with subsequent focal expansion, resulting in status spongiosus, disruption, dilatation, rhexis, and phagocytosis. Based on these results, WHS is best described as a “spongy myelinopathy” with widespread central nervous system involvement.

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