Choristoma of the Optic Nerve: Neuroimaging Characteristics and Association with Spinal Cord Lipoma

1998 ◽  
Vol 212 (3) ◽  
pp. 180-183 ◽  
Author(s):  
Albert Daxer ◽  
Ulrike Sailer ◽  
Armin Ettl ◽  
Gerald Bleckenwegner ◽  
Stephan Felber
Keyword(s):  
Spinal Cord ◽  
Optic Nerve ◽  
Cord Lipoma

METABOLIC STUDIES WITH 131I-LABELED THYROXINE. II.

1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Optic Nerve ◽  
Pituitary Gland ◽  
Time Interval ◽  
Time Intervals ◽  
Pituitary Glands ◽  
The Central Nervous System ◽  
Tentative Explanation

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.

Comparison of clinical, immunological and neuroimaging features between anti-aquaporin-4 antibody-positive and antibody-negative Sjögren’s syndrome patients with central nervous system manifestations

2012 ◽  
Vol 18 (6) ◽  
pp. 807-816 ◽  
Author(s):  
Riwanti Estiasari ◽  
Takuya Matsushita ◽  
Katsuhisa Masaki ◽  
Takuya Akiyama ◽  
Tomomi Yonekawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Optic Nerve ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Posterior Column ◽  
Aquaporin 4 ◽  
Aqp4 Antibody ◽  
Sjögren‘S Syndrome

Background and objective: The objective of this study is to clarify clinical, immunological, and neuroimaging features in anti-aquaporin-4 (AQP4) antibody-positive and antibody-negative Sjögren’s syndrome (SS) patients with central nervous system (CNS) involvement. Methods: Medical records and MRI scans were retrospectively analyzed in 22 consecutive SS patients with CNS manifestations. Results: Seven (31.8%) patients were positive for anti-AQP4 antibodies. The frequency of visual impairment was higher in anti-AQP4 antibody-positive patients than in antibody-negative patients (71.4% vs. 0.0%, p = 0.0008). Brain MRI showed that discrete lesions were more commonly found in the cerebrum, brainstem, and optic nerve in anti-AQP4 antibody-positive patients than in antibody-negative patients ( p = 0.002, p = 0.006, and p = 0.004, respectively), while spinal cord MRI showed that posterior column lesions in the cervical spinal cord were more frequent in anti-AQP4 antibody-positive patients than in antibody-negative patients (71.4% vs. 14.3%, p = 0.01). SS-A antibody titers were higher in anti-AQP4 antibody-positive patients than in antibody-negative patients ( p = 0.012) and were also higher in patients with longitudinally extensive spinal cord lesions (LESCLs) than in those without LESCLs ( p = 0.019). Conclusions: In SS, the presence of anti-AQP4 antibodies is associated with involvement of the optic nerve, cerebrum and brainstem, and with cervical posterior column lesions in the spinal cord.

DETERMINATION OF THE LIPID BASES IN THE LIPIDS OF SPINAL CORD, OPTIC NERVE AND SCIATIC NERVE OF SOME SPECIES

1967 ◽  
pp. 325-337 ◽  
Author(s):  
G. SCHMIDT ◽  
E.L. HOGAN ◽  
A. KJETA-FYDA ◽  
T. TANAKA ◽  
J. JOSEPH ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Optic Nerve ◽  
Sciatic Nerve

scholarly journals Asymptomatic spinal cord lesions in clinically isolated optic nerve, brain stem, and spinal cord syndromes suggestive of demyelination

1998 ◽  
Vol 64 (3) ◽  
pp. 353-357 ◽  
Author(s):  
J I O'Riordan ◽  
N A Losseff ◽  
C Phatouros ◽  
A J Thompson ◽  
I F Moseley ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Optic Nerve ◽  
Brain Stem ◽  
Spinal Cord Lesions

scholarly journals Protective effect of an elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin oligodendroglial glycoprotein

2012 ◽  
Vol 18 (4) ◽  
pp. 398-408 ◽  
Author(s):  
Katja Herges ◽  
Brigit A de Jong ◽  
Ilan Kolkowitz ◽  
Caitlin Dunn ◽  
Gil Mandelbaum ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Optic Nerve ◽  
Neuromyelitis Optica ◽  
Neutrophil Elastase ◽  
Th17 Cells ◽  
Neutrophil Elastase Inhibitor ◽  
Elastase Inhibitor ◽  
Sivelestat Sodium Hydrate ◽  
Th17 Cytokines ◽  
Sivelestat Sodium

Background: The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-β treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with Th17 cells is exacerbated by IFN-β, in contrast to disease induced with Th1 where treatment attenuated symptoms. Objective: This study demonstrates the similarities between NMO and Th17 EAE and how neutrophils mediate pathology in Th17 disease. Methods: Levels of blood biomarkers in NMO were assessed by Luminex and ELISA. Effects of IFN-β on neutrophils were assessed by culture assays and immunofluorescence. EAE was induced by transfer of myelin-specific Th1 or Th17 cells and treated with Sivelestat sodium hydrate, a neutrophil elastase inhibitor. Results: We show Th17 cytokines, granulocyte chemokines, type 1 interferon and neutrophil elastase are elevated in patients with definitive NMO. In culture, we find that IFN-β stimulates neutrophils to release neutrophil elastase. In Th17 EAE, we demonstrate neutrophilic infiltration in the optic nerve and spinal cord which was not present in Th1 EAE. Blockade of neutrophil elastase with Sivelestat had efficacy in Th17 EAE but not Th1 EAE. Conclusions: The similarities between Th17 EAE and NMO indicate that this model represents several aspects of NMO. Neutrophils are critical in the pathologies of both Th17-EAE and NMO, and therefore blockade of neutrophil elastase is a promising target in treating NMO.

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